Myd88

Summary

Gene Symbol: Myd88
Description: myeloid differentiation primary response gene 88
Alias: myeloid differentiation primary response protein MyD88, myeloid differentiation primary response protein 88
Species: mouse

Top Publications

  1. ncbi Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis
    Seth Rakoff-Nahoum
    Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA
    Cell 118:229-41. 2004
  2. pmc Innate immunity and intestinal microbiota in the development of Type 1 diabetes
    Li Wen
    Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nature 455:1109-13. 2008
  3. ncbi Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway
    Masahiro Yamamoto
    Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3 1 Yamada oka, Suita Osaka 565 0871, Japan
    Science 301:640-3. 2003
  4. ncbi IRF-7 is the master regulator of type-I interferon-dependent immune responses
    Kenya Honda
    Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Hongo 7 3 1, Bunkyo ku, Tokyo 113 0033, Japan
    Nature 434:772-7. 2005
  5. ncbi Toll-like receptors control activation of adaptive immune responses
    M Schnare
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    Nat Immunol 2:947-50. 2001
  6. ncbi Species-specific recognition of single-stranded RNA via toll-like receptor 7 and 8
    Florian Heil
    Institute of Medical Microbiology, Immunology and Hygiene, Technische Universitat Munchen, Trogerstr 9, D 81675 Munich, Germany
    Science 303:1526-9. 2004
  7. pmc Microbiota-induced IL-1β, but not IL-6, is critical for the development of steady-state TH17 cells in the intestine
    Michael H Shaw
    Department of Pathology and Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, MI 48109, USA
    J Exp Med 209:251-8. 2012
  8. ncbi Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection
    O Takeuchi
    Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan Core Research for Evolutional Science and Technology of Japan Science and Technology Corporation, Osaka, Japan
    J Immunol 165:5392-6. 2000
  9. pmc Demonstration of inflammation-induced cancer and cancer immunoediting during primary tumorigenesis
    Jeremy B Swann
    Cancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Victoria 3002, Australia
    Proc Natl Acad Sci U S A 105:652-6. 2008
  10. pmc MyD88 signaling in the CNS is required for development of fatty acid-induced leptin resistance and diet-induced obesity
    Andre Kleinridders
    Department of Mouse Genetics and Metabolism, Institute for Genetics, Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases CECAD and Center of Molecular Medicine Cologne CMMC, University of Cologne, D 50674 Cologne, Germany
    Cell Metab 10:249-59. 2009

Research Grants

Detail Information

Publications224 found, 100 shown here

  1. ncbi Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis
    Seth Rakoff-Nahoum
    Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA
    Cell 118:229-41. 2004
    ..These findings reveal a novel function of TLRs-control of intestinal epithelial homeostasis and protection from injury-and provide a new perspective on the evolution of host-microbial interactions...
  2. pmc Innate immunity and intestinal microbiota in the development of Type 1 diabetes
    Li Wen
    Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nature 455:1109-13. 2008
    ..Here we show that specific pathogen-free NOD mice lacking MyD88 protein (an adaptor for multiple innate immune receptors that recognize microbial stimuli) do not develop T1D...
  3. ncbi Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway
    Masahiro Yamamoto
    Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3 1 Yamada oka, Suita Osaka 565 0871, Japan
    Science 301:640-3. 2003
    Stimulation of Toll-like receptors (TLRs) triggers activation of a common MyD88-dependent signaling pathway as well as a MyD88-independent pathway that is unique to TLR3 and TLR4 signaling pathways leading to interferon (IFN)-beta ..
  4. ncbi IRF-7 is the master regulator of type-I interferon-dependent immune responses
    Kenya Honda
    Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Hongo 7 3 1, Bunkyo ku, Tokyo 113 0033, Japan
    Nature 434:772-7. 2005
    ..plasmacytoid dendritic cells by the Toll-like receptor 9 (TLR9) subfamily, which generates signals via the adaptor MyD88 to elicit robust IFN induction...
  5. ncbi Toll-like receptors control activation of adaptive immune responses
    M Schnare
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    Nat Immunol 2:947-50. 2001
    ..patterns and initiating the activation of NF-kappaB and other signaling pathways through the adapter protein, MyD88. Here we show that MyD88-deficient mice have a profound defect in the activation of antigen-specific T helper type ..
  6. ncbi Species-specific recognition of single-stranded RNA via toll-like receptor 7 and 8
    Florian Heil
    Institute of Medical Microbiology, Immunology and Hygiene, Technische Universitat Munchen, Trogerstr 9, D 81675 Munich, Germany
    Science 303:1526-9. 2004
    ..These data suggest that ssRNA represents a physiological ligand for TLR7 and TLR8...
  7. pmc Microbiota-induced IL-1β, but not IL-6, is critical for the development of steady-state TH17 cells in the intestine
    Michael H Shaw
    Department of Pathology and Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, MI 48109, USA
    J Exp Med 209:251-8. 2012
    ..In the absence of IL-1β-IL-1R or MyD88 signaling, there is a selective reduction in the frequency of intestinal sT(H)17 cells and impaired production of ..
  8. ncbi Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection
    O Takeuchi
    Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan Core Research for Evolutional Science and Technology of Japan Science and Technology Corporation, Osaka, Japan
    J Immunol 165:5392-6. 2000
    ..b>MyD88 is shown to be an adaptor molecule essential for TLR family signaling...
  9. pmc Demonstration of inflammation-induced cancer and cancer immunoediting during primary tumorigenesis
    Jeremy B Swann
    Cancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Victoria 3002, Australia
    Proc Natl Acad Sci U S A 105:652-6. 2008
    ..the effects of loss of the Toll-like receptor-associated signaling adaptor myeloid-differentiation factor 88 (MyD88) on tumor induction in two distinct mouse models of carcinogenesis...
  10. pmc MyD88 signaling in the CNS is required for development of fatty acid-induced leptin resistance and diet-induced obesity
    Andre Kleinridders
    Department of Mouse Genetics and Metabolism, Institute for Genetics, Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases CECAD and Center of Molecular Medicine Cologne CMMC, University of Cologne, D 50674 Cologne, Germany
    Cell Metab 10:249-59. 2009
    ..resistance and diet-induced obesity in vivo, we have characterized mice deficient for the TLR adaptor molecule MyD88 in the CNS (MyD88(DeltaCNS))...
  11. pmc The beta-glucan receptor dectin-1 functions together with TLR2 to mediate macrophage activation by mycobacteria
    Mahesh Yadav
    Department of Biological Sciences, Center for Tropical Disease Research and Training, University of Notre Dame, 130 Galvin Life Science Center, Notre Dame, IN 46556, USA
    Blood 108:3168-75. 2006
    ..study, we used bone marrow-derived macrophages isolated from mannose receptor (MR), complement receptor 3 (CR3), MyD88, Toll-like receptor 4 (TLR4), and TLR2 knockout mice to examine the significance of these receptors in mediating a ..
  12. pmc The ubiquitin-editing enzyme A20 restricts nucleotide-binding oligomerization domain containing 2-triggered signals
    Osamu Hitotsumatsu
    UCSF Colitis Center, Gastroenterology Division, Department of Medicine, Program in Biomedical Sciences, University of California at San Francisco, San Francisco, CA 94143 0538, USA
    Immunity 28:381-90. 2008
    ..These exaggerated responses occur independently of the TLR adaptors MyD88 and TRIF as well as TNF signals...
  13. ncbi Toll-like receptor 9-dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE
    Jane Tian
    Inflammation and Autoimmune Group, Research Department, MedImmune, Gaithersburg, Maryland 20878, USA
    Nat Immunol 8:487-96. 2007
    ..was an essential component of DNA-containing immune complexes that stimulated cytokine production through a TLR9-MyD88 pathway involving the multivalent receptor RAGE...
  14. ncbi Gout-associated uric acid crystals activate the NALP3 inflammasome
    Fabio Martinon
    Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, 1066 Epalinges, Switzerland
    Nature 440:237-41. 2006
    ..These findings provide insight into the molecular processes underlying the inflammatory conditions of gout and pseudogout, and further support a pivotal role of the inflammasome in several autoinflammatory diseases...
  15. pmc Recognition of single-stranded RNA viruses by Toll-like receptor 7
    Jennifer M Lund
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 101:5598-603. 2004
    ..Mice deficient in either the TLR7 or the TLR adaptor protein MyD88 demonstrated reduced responses to in vivo infection with vesicular stomatitis virus...
  16. pmc Syk kinase is required for collaborative cytokine production induced through Dectin-1 and Toll-like receptors
    Kevin M Dennehy
    Institute of Infectious Disease and Molecular Medicine, Clinical Laboratory Sciences Division of Immunology, University of Cape Town, Cape Town, South Africa
    Eur J Immunol 38:500-6. 2008
    ..Deficiency of either Syk or the TLR adaptor MyD88 abolished collaborative responses, which include TNF, MIP-1alpha and MIP-2 production, and which are comparable to ..
  17. ncbi TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells
    Marc Veldhoen
    Division of Molecular Immunology, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, United Kingdom
    Immunity 24:179-89. 2006
    ..Our data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation of IL-17-producing T cells...
  18. doi Bacterial recognition by TLR7 in the lysosomes of conventional dendritic cells
    Giuseppe Mancuso
    The Elie Metchnikoff Department, University of Messina, Messina, Italy
    Nat Immunol 10:587-94. 2009
    ..induced interferon in conventional dendritic cells by a mechanism that required Toll-like receptor 7, the adaptor MyD88 and the transcription factor IRF1, all of which localized together with bacterial products in degradative vacuoles ..
  19. pmc Direct recognition of the mycobacterial glycolipid, trehalose dimycolate, by C-type lectin Mincle
    Eri Ishikawa
    Division of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
    J Exp Med 206:2879-88. 2009
    ..Whole mycobacteria were able to activate macrophages even in MyD88-deficient background, but the activation was significantly diminished in Mincle/MyD88 double-deficient macrophages...
  20. pmc Cutting edge: Mincle is essential for recognition and adjuvanticity of the mycobacterial cord factor and its synthetic analog trehalose-dibehenate
    Hanne Schoenen
    Institute of Clinical Microbiology, Immunology and Hygiene Medical Department, Friedrich Alexander Universität Erlangen Nürnberg and University Clinics of Erlangen, Erlangen, Germany
    J Immunol 184:2756-60. 2010
    ..These results establish that Mincle is a key receptor for the mycobacterial cord factor and controls the Th1/Th17 adjuvanticity of TDM and TDB...
  21. pmc Lipopolysaccharide signaling without a nucleus: kinase cascades stimulate platelet shedding of proinflammatory IL-1β-rich microparticles
    G Thomas Brown
    Medical Scientist Training Program, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA
    J Immunol 186:5489-96. 2011
    ..inhibitors, cell-penetrating chimeric peptide inhibitors, and gene-targeted animals to show splicing required MyD88 and TIRAP, and IRAK1/4, Akt, and JNK phosphorylation and activation...
  22. ncbi Small anti-viral compounds activate immune cells via the TLR7 MyD88-dependent signaling pathway
    Hiroaki Hemmi
    Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3 1 Yamada oka, Suita, Osaka 565 0871, Japan
    Nat Immunol 3:196-200. 2002
    ..Here we show that the imidazoquinolines activate immune cells via the Toll-like receptor 7 (TLR7)-MyD88-dependent signaling pathway...
  23. ncbi Innate antiviral responses by means of TLR7-mediated recognition of single-stranded RNA
    Sandra S Diebold
    Immunobiology Laboratory, Cancer Research UK, London Research Institute, London WC2A 3PX, UK
    Science 303:1529-31. 2004
    ..requires endosomal recognition of influenza genomic RNA and signaling by means of Toll-like receptor 7 (TLR7) and MyD88. Single-stranded RNA (ssRNA) molecules of nonviral origin also induce TLR7-dependent production of inflammatory ..
  24. ncbi Regulation of lung injury and repair by Toll-like receptors and hyaluronan
    Dianhua Jiang
    Department of Medicine, Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520, USA
    Nat Med 11:1173-9. 2005
    ..Here we report that hyaluronan degradation products require MyD88 and both Toll-like receptor (TLR)4 and TLR2 in vitro and in vivo to initiate inflammatory responses in acute lung ..
  25. ncbi Toll-like receptors modulate adult hippocampal neurogenesis
    Asya Rolls
    Department of Neurobiology, The Weizmann Institute of Science, 76100 Rehovot, Israel
    Nat Cell Biol 9:1081-8. 2007
    ..The activation of TLRs on the NPCs was mediated via MyD88 and induced PKCalpha/beta-dependent activation of the NF-kappaB signalling pathway...
  26. pmc Caspase-1 independent IL-1beta production is critical for host resistance to mycobacterium tuberculosis and does not require TLR signaling in vivo
    Katrin D Mayer-Barber
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 184:3326-30. 2010
    To investigate the respective contributions of TLR versus IL-1R mediated signals in MyD88 dependent control of Mycobacterium tuberculosis, we compared the outcome of M...
  27. ncbi TLR9 signals after translocating from the ER to CpG DNA in the lysosome
    Eicke Latz
    Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Lazare Research Building 308, 364 Plantation Street, Worcester, MA 01605, USA
    Nat Immunol 5:190-8. 2004
    ..of CpG DNA in cells, TLR9 redistributes from the ER to CpG DNA-containing structures, which also accumulate MyD88. Our data indicate a previously unknown mechanism of cellular activation involving the recruitment of TLR9 from ..
  28. pmc Activation of IL-27 p28 gene transcription by interferon regulatory factor 8 in cooperation with interferon regulatory factor 1
    Jidong Zhang
    Division of Immunobiology, Department of Internal Medicine, Saint Louis University School of Medicine, St Louis, Missouri 63104, USA
    J Biol Chem 285:21269-81. 2010
    ..Lipopolysaccharide, as a potent inducer of IL-27 p28 expression, could activate IRF-8 expression in a MyD88-dependent pathway, which in turn induced p28 gene transcription through NF-kappaB and/or IRF-8...
  29. ncbi Unresponsiveness of MyD88-deficient mice to endotoxin
    T Kawai
    Department of Biochemistry, Hyogo College of Medicine, Nishinomiya, Japan
    Immunity 11:115-22. 1999
    b>MyD88 is a general adaptor protein that plays an important role in the Toll/IL-1 receptor family signalings...
  30. ncbi The contribution of the Toll-like/IL-1 receptor superfamily to innate and adaptive immunity to fungal pathogens in vivo
    Silvia Bellocchio
    Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Perugia, Italy
    J Immunol 172:3059-69. 2004
    ..In this study we evaluate the impact of the IL-1R/TLR/myeloid differentiation primary response gene 88 (MyD88)-dependent signaling pathway on the innate and adaptive Th immunities to C. albicans and A. fumigatus in vivo...
  31. ncbi Central role of MyD88-dependent dendritic cell maturation and proinflammatory cytokine production to control Brucella abortus infection
    Gilson Costa Macedo
    Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte Minas Gerais, Brazil
    J Immunol 180:1080-7. 2008
    ..The enhanced susceptibility to virulent B. abortus observed in MyD88 knockout (KO) mice led us to investigate the mechanisms involved in MyD88-dependent immune responses...
  32. pmc Mannose-binding lectin enhances Toll-like receptors 2 and 6 signaling from the phagosome
    W K Eddie Ip
    Laboratory of Developmental Immunology, Department of Pediatrics, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA
    J Exp Med 205:169-81. 2008
    ..Furthermore, we demonstrate that this cooperation occurs within the phagosome, emphasizing the importance of engulfment in providing the appropriate cellular environment to facilitate the synergy between these defense pathways...
  33. doi Identification of oxidative stress and Toll-like receptor 4 signaling as a key pathway of acute lung injury
    Yumiko Imai
    IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Dr Bohrgasse 3, A 1030 Vienna, Austria
    Cell 133:235-49. 2008
    ..Moreover, deletion of ncf1, which controls ROS production, improves the severity of H5N1-mediated ALI. Our data identify oxidative stress and innate immunity as key lung injury pathways that control the severity of ALI...
  34. doi Mice deficient in MyD88 Develop a Th2-dominant response and severe pathology in the upper genital tract following Chlamydia muridarum infection
    Lili Chen
    Department of Microbiology and Immunology, University of Texas Health Science Center, San Antonio, TX 78229, USA
    J Immunol 184:2602-10. 2010
    b>MyD88, a key adaptor molecule required for many innate immunity receptor-activated signaling pathways, was evaluated in a Chlamydia muridarum urogenital tract infection model...
  35. pmc IL-1α modulates neutrophil recruitment in chronic inflammation induced by hydrocarbon oil
    Pui Y Lee
    Division of Rheumatology and Clinical Immunology, University of Florida, Gainesville, FL 32610, USA
    J Immunol 186:1747-54. 2011
    ..is dependent on a different pathway requiring TLR-7, type I IFN receptor, and CCR2, the adaptor molecules MyD88, IL-1R-associated kinase (IRAK)-4, IRAK-1, and IRAK-2 are shared in regulating the recruitment of both monocytes ..
  36. pmc Induction of COX-2 enzyme and down-regulation of COX-1 expression by lipopolysaccharide (LPS) control prostaglandin E2 production in astrocytes
    Miriam Font-Nieves
    Department of Brain Ischemia and Neurodegeneration, Institute for Biomedical Research of Barcelona, Consejo Superior de Investigaciones Cientificas, Institut d Investigacions Biomediques August Pi i Sunyer, 08036 Barcelona, Spain
    J Biol Chem 287:6454-68. 2012
    ..astrocytes, LPS strongly induced COX-2 and microsomal prostaglandin-E(2) (PGE(2)) synthase-1, mediated by the MyD88-dependent NFκB pathway and influenced by mitogen-activated protein kinase pathways...
  37. ncbi Impaired production of proinflammatory cytokines and host resistance to acute infection with Trypanosoma cruzi in mice lacking functional myeloid differentiation factor 88
    Marco A Campos
    Department of Biochemistry and Immunology, Instituto de Ciencias Biologicas, and School of Pharmacy, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil
    J Immunol 172:1711-8. 2004
    ..Here, we evaluated the impact of TLR2 and myeloid differentiation factor 88 (MyD88) deficiencies in host resistance to infection with T. cruzi...
  38. pmc MyD88-deficient mice display a profound loss in resistance to Mycobacterium tuberculosis associated with partially impaired Th1 cytokine and nitric oxide synthase 2 expression
    Charles A Scanga
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Infect Immun 72:2400-4. 2004
    ..b>MyD88(-/-) mice were used to examine whether TLRs play any role in protection against aerogenic M...
  39. ncbi MyD88-dependent and -independent murine cytomegalovirus sensing for IFN-alpha release and initiation of immune responses in vivo
    Thomas Delale
    Schering Plough, Laboratory for Immunological Research, Dardilly, France
    J Immunol 175:6723-32. 2005
    ..Upon murine CMV (MCMV) infection, both MyD88-/- and TLR9-/- mice were more susceptible and presented increased viral loads compared with C57BL/6, TLR2-/-, TLR3-..
  40. doi Toll/IL-1 signaling is critical for house dust mite-specific helper T cell type 2 and type 17 [corrected] responses
    Simon Phipps
    Centre for Asthma and Respiratory Diseases, School of Biomedical Sciences, University of Newcastle, NSW, 2300 Australia
    Am J Respir Crit Care Med 179:883-93. 2009
    ....
  41. ncbi IL-1 receptor-mediated signal is an essential component of MyD88-dependent innate response to Mycobacterium tuberculosis infection
    Cecile M Fremond
    University of Orleans, Centre National de la Recherche Scientifique, Molecular Immunology and Embryology, Orleans, France
    J Immunol 179:1178-89. 2007
    b>MyD88, the common adapter involved in TLR, IL-1, and IL-18 receptor signaling, is essential for the control of acute Mycobacterium tuberculosis (MTB) infection...
  42. ncbi Genetically resistant mice lacking MyD88-adapter protein display a high susceptibility to Leishmania major infection associated with a polarized Th2 response
    Eric Muraille
    Laboratory of Parasitology, Universite Libre de Bruxelles, Erasme, Belgium
    J Immunol 170:4237-41. 2003
    ..Myeloid differentiation marker 88 (MyD88) is an adaptator protein that links the IL-1/Toll-like receptor family to IL-1R-associated protein kinase...
  43. pmc Toll-like receptor 9 mediates innate immune activation by the malaria pigment hemozoin
    Cevayir Coban
    Exploratory Research for Advanced Technology ERATO, Japan Science and Technology Agency JST, Osaka, Japan
    J Exp Med 201:19-25. 2005
    ..Such responses were severely impaired in TLR9-/- and myeloid differentiation factor 88 (MyD88)-/-, but not in TLR2, TLR4, TLR7, or Toll/interleukin 1 receptor domain-containing adaptor-inducing interferon ..
  44. ncbi Syk-dependent cytokine induction by Dectin-1 reveals a novel pattern recognition pathway for C type lectins
    Neil C Rogers
    Immunobiology Laboratory, Cancer Research UK, London Research Institute, 44 Lincoln s Inn Fields, London WC2A 3PX, United Kingdom
    Immunity 22:507-17. 2005
    ..These results identify a novel signaling pathway involved in pattern recognition by C type lectins and suggest a potential role for Syk kinase in regulation of innate immunity...
  45. ncbi Control of B-cell responses by Toll-like receptors
    Chandrashekhar Pasare
    Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, 300 Cedar Street New Haven, Connecticut 06510, USA
    Nature 438:364-8. 2005
    ..We find that, in addition to CD4+ T-cell help, generation of T-dependent antigen-specific antibody responses requires activation of TLRs in B cells...
  46. pmc Both TRIF- and MyD88-dependent signaling contribute to host defense against pulmonary Klebsiella infection
    Shanshan Cai
    Department of Pathobiological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA
    J Immunol 183:6629-38. 2009
    Klebsiella pneumoniae causes extensive lung damage. TLR signaling involves adaptors TRIF and MyD88. However, the relative contribution of TRIF and MyD88 signaling in host defense against pulmonary K...
  47. doi Astrocytes initiate inflammation in the injured mouse spinal cord by promoting the entry of neutrophils and inflammatory monocytes in an IL-1 receptor/MyD88-dependent fashion
    Isabelle Pineau
    Department of Molecular Medicine, Laval University, Quebec, Quebec, Canada G1V 4G2
    Brain Behav Immun 24:540-53. 2010
    ..Interestingly, astrocytes from mice deficient in MyD88 signaling produced significantly less MCP-1 and MIP-2 and were unable to synthesize KC...
  48. pmc Distinct roles for Dectin-1 and TLR4 in the pathogenesis of Aspergillus fumigatus keratitis
    Sixto M Leal
    Department of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, Ohio, United States of America
    PLoS Pathog 6:e1000976. 2010
    ..We also found that TRIF(-/-) and TIRAP(-/-) mice exhibited no fungal-killing defects, but that MyD88(-/-) and IL-1R1(-/-) mice were unable to regulate fungal growth...
  49. pmc Dual function of MyD88 in RAS signaling and inflammation, leading to mouse and human cell transformation
    Isabelle Coste
    CNRS UMR5201, University of Lyon, Centre Leon Berard, Lyon, France
    J Clin Invest 120:3663-7. 2010
    Accumulating evidence points to inflammation as a promoter of carcinogenesis. MyD88 is an adaptor molecule in TLR and IL-1R signaling that was recently implicated in tumorigenesis through proinflammatory mechanisms...
  50. pmc Selective utilization of Toll-like receptor and MyD88 signaling in B cells for enhancement of the antiviral germinal center response
    Baidong Hou
    Department of Microbiology and Immunology, University of California, San Francisco, CA 94143, USA
    Immunity 34:375-84. 2011
    ..to T cell-dependent (TD) antibody responses was assessed by using mice lacking the TLR signaling adaptor MyD88 in individual cell types...
  51. ncbi Identification of Lps2 as a key transducer of MyD88-independent TIR signalling
    K Hoebe
    Department of Immunology, IMM 31, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA
    Nature 424:743-8. 2003
    ..Compound homozygosity for mutations at Trif and MyD88 (a cytoplasmic TIR-domain-containing adaptor protein) loci ablates all responses to LPS, indicating that only two ..
  52. ncbi Integral role of IRF-5 in the gene induction programme activated by Toll-like receptors
    Akinori Takaoka
    Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Hongo 7 3 1, Bunkyo ku, Tokyo 113 0033, Japan
    Nature 434:243-9. 2005
    The activation of Toll-like receptors (TLRs) is central to innate and adaptive immunity. All TLRs use the adaptor MyD88 for signalling, but the mechanisms underlying the MyD88-mediated gene induction programme are as yet not fully ..
  53. ncbi A Toll-like receptor-independent antiviral response induced by double-stranded B-form DNA
    Ken J Ishii
    Exploratory Research for Advanced Technology, Japan Science and Technology Agency, Research Institute for Microbial Diseases, Osaka University, Osaka 565 0871, Japan
    Nat Immunol 7:40-8. 2006
    ..These results suggest that both TBK1 and IKKi are required for innate immune activation by B-DNA, which might be important in antiviral innate immunity and other DNA-associated immune disorders...
  54. ncbi Recognition of cytosolic DNA activates an IRF3-dependent innate immune response
    Daniel B Stetson
    Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Immunity 24:93-103. 2006
    ..These findings define an innate immune response to DNA linked to type I interferon production...
  55. pmc Dendritic cells prime natural killer cells by trans-presenting interleukin 15
    Mathias Lucas
    Skirball Institute of Biomolecular Medicine, Program in Molecular Pathogenesis, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA
    Immunity 26:503-17. 2007
    ..Our data define a unique in vivo role of DCs for the priming of NK cells, revealing a striking and previously unappreciated homology to T lymphocytes of the adaptive immune system...
  56. pmc Regulation of hierarchical clustering and activation of innate immune cells by dendritic cells
    Suk Jo Kang
    Howard Hughes Medical Institute, Department of Medicine, University of California, San Francisco, San Francisco, CA 94143 0795, USA
    Immunity 29:819-33. 2008
    ..and required pertussis-toxin-sensitive recruitment, in part mediated by the chemokine receptor CCR5, and MyD88 adaptor-mediated signaling...
  57. pmc The major component in schistosome eggs responsible for conditioning dendritic cells for Th2 polarization is a T2 ribonuclease (omega-1)
    Svenja Steinfelder
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Exp Med 206:1681-90. 2009
    ..The Th2-promoting activity of omega-1 was found to be sensitive to ribonuclease inhibition and did not require MyD88/TRIF signaling in DCs...
  58. pmc Murine toll-like receptor 2 activation induces type I interferon responses from endolysosomal compartments
    Nicole Dietrich
    Molecular Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany
    PLoS ONE 5:e10250. 2010
    ..Until now, TLR2 activation by bacterial ligands has long been associated with pro-inflammatory cytokines but not type I interferon responses...
  59. pmc Caspase-1 dependent IL-1β secretion is critical for host defense in a mouse model of Chlamydia pneumoniae lung infection
    Kenichi Shimada
    Division of Pediatrics Infectious Disease and Immunology, Cedars Sinai Medical Center and David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, United States of America
    PLoS ONE 6:e21477. 2011
    ..In vitro investigation reveals that CP-induced IL-1β secretion by macrophages requires TLR2/MyD88 and NLRP3/ASC/Caspase-1 signaling...
  60. doi IL-1 blockade attenuates islet amyloid polypeptide-induced proinflammatory cytokine release and pancreatic islet graft dysfunction
    Clara Westwell-Roper
    Department of Pathology and Laboratory Medicine, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4
    J Immunol 187:2755-65. 2011
    ..hIAPP-induced TNF-α secretion was markedly diminished in MyD88-, but not TLR2- or TLR4-deficient macrophages, and in cells treated with the IL-1R antagonist (IL-1Ra) anakinra...
  61. pmc Interleukin-1 receptor-associated kinase 4 is essential for initial host control of Brucella abortus infection
    Fernanda S Oliveira
    Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil
    Infect Immun 79:4688-95. 2011
    ..depends on myeloid differentiation factor 88 (MyD88) signaling...
  62. doi The IκB kinase complex regulates the stability of cytokine-encoding mRNA induced by TLR-IL-1R by controlling degradation of regnase-1
    Hidenori Iwasaki
    Laboratory of Host Defense, World Premier International Immunology Frontier Research Center, Osaka University, Osaka, Japan
    Nat Immunol 12:1167-75. 2011
    ..Our data demonstrate that the IKK complex phosphorylates not only IκBα, thereby activating transcription, but also regnase-1, thereby releasing a 'brake' on IL-6 mRNA expression...
  63. pmc Toll-like receptor 3 is a potent negative regulator of axonal growth in mammals
    Jill S Cameron
    Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA
    J Neurosci 27:13033-41. 2007
    ....
  64. pmc TANK is a negative regulator of Toll-like receptor signaling and is critical for the prevention of autoimmune nephritis
    Tatsukata Kawagoe
    Laboratory of Host Defense, World Premier International Immunology Frontier Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan
    Nat Immunol 10:965-72. 2009
    ..in Tank(-/-) mice was abrogated by antibiotic treatment or the absence of interleukin 6 (IL-6) or the adaptor MyD88. Our results demonstrate that constitutive TLR signaling by intestinal commensal microflora is suppressed by TANK.
  65. doi TLR-2-activated B cells suppress Helicobacter-induced preneoplastic gastric immunopathology by inducing T regulatory-1 cells
    Ayca Sayi
    Institute of Molecular Cancer Research, University of Zurich, Zurich 8057, Switzerland
    J Immunol 186:878-90. 2011
    ..Adoptive cotransfer of MyD88-proficient B cells and Tr-1 cells restores a normal gastric mucosal architecture in MyD88(-/-) and IL-10(-/-) mice ..
  66. ncbi Syk- and CARD9-dependent coupling of innate immunity to the induction of T helper cells that produce interleukin 17
    Salome Leibundgut-Landmann
    Immunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln s Inn Fields Laboratories, London WC2A 3PX, UK
    Nat Immunol 8:630-8. 2007
    ..Our data indicate that signaling through Syk and CARD9 can couple innate to adaptive immunity independently of Toll-like receptor signals and that CARD9 is required for the development of T(H)-17 responses to some pathogens...
  67. ncbi Restriction of Legionella pneumophila growth in macrophages requires the concerted action of cytokine and Naip5/Ipaf signalling pathways
    Jorn Coers
    Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
    Cell Microbiol 9:2344-57. 2007
    ..pneumophila is more complex than previously appreciated, and involves the concerted action of cytokine and intracellular microbe sensor signalling pathways...
  68. pmc MyD88 and Trif target Beclin 1 to trigger autophagy in macrophages
    Chong Shan Shi
    B Cell Molecular Immunology Section, Laboratory of Immunoregulation, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 283:33175-82. 2008
    ..that not only TLR4, but also other TLR family members induce autophagy in macrophages, which is inhibited by MyD88, Trif, or Beclin 1 shRNA expression...
  69. pmc Type I interferon production enhances susceptibility to Listeria monocytogenes infection
    Ryan M O'Connell
    Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, 8 240 Factor Bldg, 10833 Le Conte Ave, 90095, USA
    J Exp Med 200:437-45. 2004
    ..Thus, our results highlight the disparate roles of type I IFNs during bacterial versus viral infections and stress the importance of proper IFN modulation in host defense...
  70. pmc Toll-like receptors on hematopoietic progenitor cells stimulate innate immune system replenishment
    Yoshinori Nagai
    Immunobiology and Cancer Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA
    Immunity 24:801-12. 2006
    ..TLR signaling via the Myd88 adaptor protein drove differentiation of myeloid progenitors, bypassing some normal growth and differentiation ..
  71. ncbi Interferon-alpha induction through Toll-like receptors involves a direct interaction of IRF7 with MyD88 and TRAF6
    Taro Kawai
    ERATO, Akira Innate Immunity Program, Japan Science and Technology Agency, Research Institute for Microbial Diseases, Osaka University, 3 1 Yamada oka, Suita, Osaka 565 0871, Japan
    Nat Immunol 5:1061-8. 2004
    ..Production of IFN-alpha is dependent on the Toll-interleukin-1 receptor domain-containing adaptor MyD88. Here we show that MyD88 formed a complex with the transcription factor IRF7 but not with IRF3...
  72. pmc Dynamic regulation of pro- and anti-inflammatory cytokines by MAPK phosphatase 1 (MKP-1) in innate immune responses
    Hongbo Chi
    Section of Immunobiology, Department of Pharmacology, and Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 103:2274-9. 2006
    ..was transiently induced by TLR stimulation through pathways mediated by both myeloid differentiation factor 88 (MyD88) and TIR domain-containing adaptor inducing IFN-beta (TRIF)...
  73. ncbi Dectin-1 and TLRs permit macrophages to distinguish between different Aspergillus fumigatus cellular states
    Geoffrey M Gersuk
    Fred Hutchinson Cancer Research Center, University of Washington, 1100 Fairview Avenue North, Seattle, WA 98109, USA
    J Immunol 176:3717-24. 2006
    ..Dectin-1 recognition of germ tubes also stimulates TNF-alpha production in the absence of both TLR2 and MyD88 signaling...
  74. ncbi Differential involvement of TLR2 and TLR4 in host survival during pulmonary infection with Chlamydia pneumoniae
    Nuria Rodriguez
    Institute of Medical Microbiology, Immunology and Hygiene, Technical University of Munich, Munich, Germany
    Eur J Immunol 36:1145-55. 2006
    ..All TLR2(-/-) x TLR4(d/d) mice succumbed to the infection, while about 50% of TLR2(-/-) mice died. Taken together, the function of TLR2 and TLR4 is required to survive pulmonary infection with C. pneumoniae...
  75. ncbi Cutting edge: TLR9 and TLR2 signaling together account for MyD88-dependent control of parasitemia in Trypanosoma cruzi infection
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 177:3515-9. 2006
    ..Strikingly, infected Tlr2(-/-)Tlr9(-/-) mice developed a parasitemia equivalent to animals lacking MyD88, an essential signaling molecule for most TLR, but did not show the acute mortality displayed by MyD88(-/-) ..
  76. pmc The innate immune responses of colonic epithelial cells to Trichuris muris are similar in mouse strains that develop a type 1 or type 2 adaptive immune response
    Matthew L deSchoolmeester
    Faculty of Life Sciences, Michael Smith Building, University of Manchester, Oxford Road, Manchester, M13 9PT, United Kingdom
    Infect Immun 74:6280-6. 2006
    ..These increases were ablated in MyD88-/- mice, and NF-kappaB p65 was phosphorylated in response to T...
  77. ncbi Mass spectrometric analysis of the endogenous type I interleukin-1 (IL-1) receptor signaling complex formed after IL-1 binding identifies IL-1RAcP, MyD88, and IRAK-4 as the stable components
    Constantinos Brikos
    Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College London, London, UK
    Mol Cell Proteomics 6:1551-9. 2007
    ..MS also enabled detection of IL-1, IL-1RI, IL-1 receptor accessory protein (IL-1RAcP), and myeloid differentiation primary response protein 88 (MyD88) in the complex...
  78. ncbi Activation of TLR2 and TLR4 by glycosylphosphatidylinositols derived from Toxoplasma gondii
    Françoise Debierre-Grockiego
    Institut fur Virologie, AG Parasitologie, Philipps University, Marburg, Germany
    J Immunol 179:1129-37. 2007
    ..b>MyD88, but not TLR2, TLR4, or CD14, is absolutely needed to trigger TNF-alpha production by macrophages exposed to T...
  79. pmc Dectin-2 recognition of house dust mite triggers cysteinyl leukotriene generation by dendritic cells
    Nora A Barrett
    Department of Medicine, Harvard Medical School, and Division of Rheumatology, Immunology, and Allergy, Brigham and Women s Hospital, Boston, MA 02115, USA
    J Immunol 182:1119-28. 2009
    ....
  80. doi Trif is not required for immune complex glomerulonephritis: dying cells activate mesangial cells via Tlr2/Myd88 rather than Tlr3/Trif
    Julia Lichtnekert
    Medizinische Poliklinik, Klinikum der Universität Innenstadt, Pettenkoferstr 8a, 80336 Munich, Germany
    Am J Physiol Renal Physiol 296:F867-74. 2009
    ..Exposure to necrotic cells activated cultured primary mesangial cells to produce Il-6 in a Tlr2/Myd88-dependent manner. Apoptotic cells activated cultured mesangial cells only when being enriched to high numbers...
  81. pmc Selective expansion of the monocytic lineage directed by bacterial infection
    Natalya V Serbina
    Infectious Disease Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, Immunology Program, Sloan Kettering Institute, New York, NY 10021, USA
    J Immunol 183:1900-10. 2009
    ..Although MyD88/Trif-mediated signaling is not required for early emigration of the mature monocyte population from the bone ..
  82. doi MYD88-dependent and -independent activation of TREM-1 via specific TLR ligands
    Heng Zheng
    Department of Veterans Affairs, Jesse Brown VA Hospital, and Department of Pharmacology, University of Illinois, Chicago, IL 60612, USA
    Eur J Immunol 40:162-71. 2010
    ..Interestingly, the expression of TREM-1 in response to LPS is not altered in myeloid differentiation factor 88 (MyD88) KO macrophages, suggesting that downstream of TLR a MyD88-independent pathway induces the expression of TREM-1...
  83. doi Recipient Toll-like receptors contribute to chronic graft dysfunction by both MyD88- and TRIF-dependent signaling
    Shijun Wang
    Department of Cellular and Molecular Pathology, German Cancer Research Center, D 69120 Heidelberg, Germany
    Dis Model Mech 3:92-103. 2010
    ..In a genetic approach to define the contribution of TLR2 and TLR4, and their adaptor proteins MyD88 and TRIF [Toll/interleukin (IL)-1 receptor domain-containing adaptor-protein inducing interferon beta], to CAD, ..
  84. pmc Stimulator of IFN gene is critical for induction of IFN-beta during Chlamydia muridarum infection
    Daniel Prantner
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    J Immunol 184:2551-60. 2010
    ..Previous studies have demonstrated no role for TLR4 and a partial role for MyD88 in chlamydial-induced IFN-beta...
  85. pmc Cutting edge: bacterial infection induces hematopoietic stem and progenitor cell expansion in the absence of TLR signaling
    Philip O Scumpia
    Department of Surgery, University of Florida College of Medicine, Gainesville, FL 32610 0286, USA
    J Immunol 184:2247-51. 2010
    ..In this study, we report that endotoxin treatment in vivo induces TLR4, MyD88, and Toll/IL-1 resistance domain-containing adaptor-inducing IFN-beta (TRIF)-dependent expansion of BM HSPCs...
  86. ncbi Myeloid differentiation factor-88 (MyD88) is essential for control of primary in vivo Francisella tularensis LVS infection, but not for control of intra-macrophage bacterial replication
    Carmen M Collazo
    Laboratory of Mycobacterial Diseases and Cellular Immunology, Division of Bacterial, Parasitic and Allergenic Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Rockville, MD 20852, USA
    Microbes Infect 8:779-90. 2006
    ..Here we wished to explore the contribution of the MyD88/Toll-like receptor signaling pathway in initiating murine responses to F. tularensis Live Vaccine Strain (LVS)...
  87. ncbi A mechanism for neurodegeneration induced by group B streptococci through activation of the TLR2/MyD88 pathway in microglia
    Seija Lehnardt
    Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    J Immunol 177:583-92. 2006
    ..from GBS (GBS-F) induce neuronal apoptosis via the activation of murine microglia through a TLR2-dependent and MyD88-dependent pathway in vitro. Microglia, astrocytes, and oligodendrocytes, but not neurons, express TLR2...
  88. ncbi RIG-I-mediated antiviral responses to single-stranded RNA bearing 5'-phosphates
    Andreas Pichlmair
    Immunobiology Laboratory, Cancer Research UK, London Research Institute, London WC2A 3PX, UK
    Science 314:997-1001. 2006
    ....
  89. ncbi Toll-like receptor signalling in macrophages links the autophagy pathway to phagocytosis
    Miguel A Sanjuan
    Department of Immunology, St Jude Children s Research Institute, Memphis, Tennessee 38105, USA
    Nature 450:1253-7. 2007
    ....
  90. pmc Group A streptococcus activates type I interferon production and MyD88-dependent signaling without involvement of TLR2, TLR4, and TLR9
    Nina Gratz
    Max F Perutz Laboratories, Department of Microbiology and Immunobiology, University of Vienna, Vienna, Austria
    J Biol Chem 283:19879-87. 2008
    ..NF-kappaB, elements of the major signaling pathways induced by TLRs, depends in most cases on the adaptor molecule MyD88. In addition, Gram-negative or intracellular bacteria elicit MyD88-independent signaling that results in ..
  91. ncbi Cutting edge: FimH adhesin of type 1 fimbriae is a novel TLR4 ligand
    Karen L Mossman
    Centre for Gene Therapeutics, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
    J Immunol 181:6702-6. 2008
    ..In this study we report that FimH induces potent innate responses in a MyD88-dependent fashion. The FimH-induced innate activity was restricted to cells expressing TLR4...
  92. pmc TANK-binding kinase-1 plays an important role during in vitro and in vivo type I IFN responses to DNA virus infections
    Andrea K Miyahira
    Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA 90095, USA
    J Immunol 182:2248-57. 2009
    ..Finally, we demonstrate the requirement for the TBK1-IFN regulatory factor-3 pathway in host defense against a DNA virus infection in vivo...
  93. ncbi Leishmania major activates IL-1 alpha expression in macrophages through a MyD88-dependent pathway
    Thomas R Hawn
    Division of Infectious Diseases, Department of Medicine, University of Washington, Seattle, WA 98195, USA
    Microbes Infect 4:763-71. 2002
    ..Transfection of macrophages with a dominant-negative version of myeloid differentiation factor 88 (MyD88), an adaptor protein which interacts with TLRs, inhibited activation of the IL-1 alpha promoter...
  94. ncbi The Salmonella pathogenicity island (SPI)-2 and SPI-1 type III secretion systems allow Salmonella serovar typhimurium to trigger colitis via MyD88-dependent and MyD88-independent mechanisms
    Siegfried Hapfelmeier
    Institute of Microbiology, D BIOL, Eidgenössiche Technische Hochschule, Zurich, Switzerland
    J Immunol 174:1675-85. 2005
    ..We studied these mechanisms in vivo using streptomycin-pretreated wild-type and knockout mice including MyD88(-/-) animals lacking an adaptor molecule required for signaling via most TLRs...
  95. ncbi Contribution of Toll-like receptor/myeloid differentiation factor 88 signaling to murine liver regeneration
    Ekihiro Seki
    First Department of Surgery, Hyogo College of Medicine, Nishinomiya, Japan
    Hepatology 41:443-50. 2005
    ..When the receptors are activated, cells bearing TLRs produce various proinflammatory cytokines in a MyD88-dependent manner...
  96. pmc MyD88-dependent signals are essential for the host immune response in experimental brain abscess
    Tammy Kielian
    Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, 4301 West Markham Street, Little Rock, AR 72205, USA
    J Immunol 178:4528-37. 2007
    ..responses to bacteria, including the majority of TLRs, the IL-1R, and the IL-18R, use a common adaptor molecule, MyD88, for transducing activation signals leading to proinflammatory mediator expression and immune effector functions...
  97. pmc Toll-like receptor 2-dependent NF-kappaB activation is involved in nontypeable Haemophilus influenzae-induced monocyte chemotactic protein 1 up-regulation in the spiral ligament fibrocytes of the inner ear
    Sung K Moon
    The Gonda Department of Cell and Molecular Biology, House Ear Institute, 2100 West 3rd Street, Los Angeles, CA 90057, USA
    Infect Immun 75:3361-72. 2007
    ..TLR2(-/-)- and MyD88(-/-)-derived SLFs revealed involvement of TLR2 and MyD88 in NTHI-induced MCP-1 up-regulation...
  98. doi B cell intrinsic MyD88 signals drive IFN-gamma production from T cells and control switching to IgG2c
    Tom A Barr
    Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh, United Kingdom
    J Immunol 183:1005-12. 2009
    ..The question of whether Ab responses to T-dependent Ags require B cell intrinsic signaling via the main TLR adaptor (MyD88) has become embroiled in confusion...
  99. ncbi Chlamydia pneumoniae stimulates IFN-gamma synthesis through MyD88-dependent, TLR2- and TLR4-independent induction of IL-18 release
    Mihai G Netea
    Department of Medicine, University Medical Center Nijmegen, The Netherlands
    J Immunol 173:1477-82. 2004
    ..In contrast, C. pneumoniae stimulated the production of IL-18 through MyD88-dependent, TLR2-, TLR4-, and CD14-independent pathways, mediated by posttranscriptional mechanisms not involving ..
  100. pmc Reciprocal regulation of IL-23 and IL-12 following co-activation of Dectin-1 and TLR signaling pathways
    Kevin M Dennehy
    Institute of Infectious Disease and Molecular Medicine, Clinical Laboratory Sciences Division of Immunology, University of Cape Town, Cape Town, South Africa
    Eur J Immunol 39:1379-86. 2009
    ..Such down-regulation occurred with multiple MyD88-coupled TLR, was dependent on signaling through Dectin-1 and also occurred in macrophages...
  101. pmc Rapid and reliable generation of invariant natural killer T-cell lines in vitro
    Asako Chiba
    Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Immunology 128:324-33. 2009
    ..Given the desire to study primary iNKT cells for many purposes, these iNKT cell lines should provide an important tool for the study of iNKT cell subsets, antigen and TCR specificity, activation, inactivation and effector functions...

Research Grants44

  1. HOST DEFENSE AGAINST INTRACELLULAR INFECTION OF THE LUNG
    Shawn Skerrett; Fiscal Year: 2005
    ..This aim will test the hypothesis that bacterial dot/icm genes direct macrophage uptake of L. pneumophila by a pathway that results in diminished cellular activation in comparison bacteria deficient in these loci. ..
  2. Induction of immunological paralysis by CpG DNA
    Ae Kyung Yi; Fiscal Year: 2008
    ..region and will determine whether CpG DNA suppresses IRAK1 expression through an endosomal pH-sensitive TLR9/MyD88-dependent pathway. We will make various mutant RAW264...
  3. Pain Mechanisms and the Development of Analgesics
    Tony Yaksh; Fiscal Year: 2006
    ..g. COX2 inhibitors, GABApentin, ziconotide) and failures (NK1 antagonist). [unreadable] [unreadable] [unreadable]..
  4. Mutagenic analysis of LPS responses
    Bruce Beutler; Fiscal Year: 2006
    ..In the case of mutations that abolish LPS tolerance, we will attempt to determine the net impact on host resistance to infection. ..
  5. Molecular Basis for Pseudomonas Recognition of Epithelia
    BARBARA KAZMIERCZAK; Fiscal Year: 2007
    ..unreadable] [unreadable]..
  6. Regulation of the Ocular Immune Response by Retinal Pigment Epithelium
    Hui Shao; Fiscal Year: 2007
    ..The results of our studies will provide new insights into the pathogenesis of uveitis. [unreadable] [unreadable] [unreadable]..
  7. Immunomodulatory Effects of Mechanical Ventilation
    WILLIAM ALTEMEIER; Fiscal Year: 2007
    ....
  8. Strategies to enhance immunity in aging
    Daniel Goldstein; Fiscal Year: 2007
    ..Goldstein to develop expertise in the biology of aging and how it relates to immunosenescence, ensuring that Dr. Goldstein will become a leading independent physician scientist in this area. [unreadable] [unreadable] [unreadable]..
  9. Innate immune responses in lymphatic filariasis
    AMY HISE; Fiscal Year: 2007
    ..abstract_text> ..
  10. Investigation of Nod2: Implications for Uveitis
    Holly Rosenzweig; Fiscal Year: 2008
    ..Together, these studies will provide valuable new information on how Nod2 is involved in autoimmunity and the pathogeneis of uveitis. ..
  11. Bacterial immunomodulation in periodontitis
    Linden Hu; Fiscal Year: 2008
    ..unreadable] [unreadable] [unreadable]..
  12. CORNEAL ENDOTHELIAL CELL IMMUNOREGULATORY FACTORS
    DALE GREGERSON; Fiscal Year: 2003
    ..identify the activity(s) to learn if it is a known factor(s); and 3. if the activity has not already been described, continue characterization of the factor(s) and mechanism of action. ..
  13. Vein wall remodeling after DVT is matrix metalloproteinase dependent
    Peter Henke; Fiscal Year: 2009
    ..This proposal will provide important mechanistic insight into the pathophysiology of post-phelbitic syndrome with real potential translation to decreasing the morbidity from this under-acknowledged disease. ..
  14. B1B lymphocytes generate T cell-independent memory
    KISHORE ALUGUPALLI; Fiscal Year: 2009
    ..Understanding the basis for the longevity of the Tl protective responses conferred by B1b cells will provide novel approaches to generate effective vaccines against pathogens expressing Tl antigens. ..
  15. Modulation of Host Cell Functions by Coxiella burnetii
    Craig R Roy; Fiscal Year: 2010
    ..These studies will elucidate pathogenic determinants that allow host cell infection by Coxiella and reveal intracellular infection strategies employed by this important pathogen. ..
  16. Local Retinal Antigen Presentation
    DALE SANNES GREGERSON; Fiscal Year: 2010
    ..dendritic cells;or 2. MHC class II on subsets of immune cells in the retina. The ability of circulating antigen presenting cells, or their precursors, to replace these deficiencies in antigen presentation will be tested. ..
  17. Genesis & Control of Lyme Disease by Innate Immunity
    Linda Bockenstedt; Fiscal Year: 2009
    ..This proposal is based on our recent findings that absence of MyD88, an intracellular adaptor molecule required for TLR-induced inflammation, does not eliminate disease in Bb-..
  18. The role of costimulatory molecules in uveitis
    Hui Shao; Fiscal Year: 2011
    ..These studies should provide insights into the pathogenic mechanism leading to disease progression and help in the development of supplementary therapies for this devastating disease. ..
  19. SIGNIFICANCE OF IMMUNOLOGICAL SEQUESTRATION IN THE EYE
    DALE SANNES GREGERSON; Fiscal Year: 2010
    ..Aim II examines the possibility that local antigen presenting cells are limiting, in number and/or function, thus contributing to retinal immune ignorance and privilege. ..
  20. Melanocortins, Energy Balance and Cancer Anorexia
    Brent Wisse; Fiscal Year: 2006
    ..Schwartz and the Harborview Medical Center Energy Metabolism Laboratory, and by joining a large community of productive researchers in the field of energy homeostasis across the University of Washington campus. ..
  21. Studies on Macrophage Resistance to Anthrax Lethal Toxin
    Molly Hughes; Fiscal Year: 2004
    ..Successful completion of these studies will yield a fundamental understanding of mechanisms of macrophage resistance to LT. ..
  22. PAIN EVOKED RELEASE OF AMINO ACIDS AND PROSTANOIDS
    Tony Yaksh; Fiscal Year: 2005
    ....
  23. Identification of E. histolytica virulence factors
    Molly Hughes; Fiscal Year: 2004
    ..Successful completion of these studies will yield a fundamental understanding of amebic proteins that interact with the E. histolytica GalNAc lectin and their role in pathogenicity. ..
  24. TOLL RECEPTORS AND CONTROL OF MAMMALIAN IMMUNITY
    Ruslan Medzhitov; Fiscal Year: 2005
    ..Our ultimate goal is to understand whether activation of different TLRs results in the induction of distinct cellular and immune responses. ..
  25. Spinal Galanin and its Receptors in Pain Processing
    Tony Yaksh; Fiscal Year: 2005
    ..We believe the outcome of these studies will provide direct evidence for the role played by this spinal peptidergic system in pain and point to the development of novel anti-hyperpathic agents. ..
  26. NEUROBIOLOGY OF PAIN
    Tony Yaksh; Fiscal Year: 2005
    ..The complexity of the problems and the diversity of the training approaches emphasize that the training received by these fellows will provide a broad base of knowledge relevant to wide areas of neurobiology. ..
  27. Development of a vaccine for murine Lyme disease
    Linden Hu; Fiscal Year: 2006
    ..burgdorferi to mice and in sterilizing infection in infected ticks. ..
  28. Interaction of HSV-1 LAT Gene & Dendritic Cells Function
    Lbachir BenMohamed; Fiscal Year: 2004
    ..a)Determine if LAT modulates cytokine and chemokine secretion by DC and chemokine-receptor expression on DC, all of which are involved in migratory activity of DC. (b)Determine if LAT changes the observed migratory activity of DC. ..
  29. ROLE OF PKD IN LEUKOCYTE ACTIVATION BY CPG DNA
    Ae Kyung Yi; Fiscal Year: 2002
    ..This proposed study would enhance our understanding of how CpG motifs in bacterial DNA break immune tolerance and contribute to chrome inflammatory autoimmune diseases such as arthritis. ..
  30. Genes that Mediate Tolerance to the Placental Allograft
    Bruce Beutler; Fiscal Year: 2006
    ..Fourth, circumvention of the toleragenic mechanism might be used to prevent normal gestation, leading to termination of pregnancy within a few days following implantation of the blastocyst. ..
  31. Thrombus resolution is CXC chemokine dependent
    Peter Henke; Fiscal Year: 2006
    ..abstract_text> ..
  32. Forward Genetic Analysis of the Innate Immune Contribution to MCMV Resistance
    Bruce Beutler; Fiscal Year: 2006
    ..unreadable] [unreadable] [unreadable]..
  33. Virulence Typing of Pseudomonas Clinical Isolates
    BARBARA KAZMIERCZAK; Fiscal Year: 2006
    ..This can have significant consequences both for public health, by limiting the emergence of multi-drug resistant pathogens in our hospitals, and for containing the cost of medical care. [unreadable] [unreadable]..
  34. Macrophage defense againt M. tuberculosis
    Jennifer Wang; Fiscal Year: 2008
    ..abstract_text> ..
  35. Role of Innate Immunity in Transplantation Tolerance
    DANIEL ROBERT GOLDSTEIN; Fiscal Year: 2010
    ..preliminary data investigate the impact of innate immunity on transplantation tolerance and show that absence of MyD88, an important TLR signal adaptor, is critical for tolerance induction...
  36. Toll-like Receptors and the Innate Immune Response
    THOMAS HAWN; Fiscal Year: 2003
    ..tuberculosis and L. major will reveal novel insights about innate immunity and infectious diseases that will have implications for vaccine development. ..
  37. Comparison of Human Ehrlichiosis Agent Genomes
    Yasuko Rikihisa; Fiscal Year: 2010
    ..chaffeensis virulence determinants and their pathogenic mechanisms. The results may point to potential chemotherapy, chemopreventive and/or vaccine candidates for treatment and prevention of human ehrlichiosis. ..
  38. CD1-Mediated Immunity Of Lyme Disease
    Linda Bockenstedt; Fiscal Year: 2005
    ..For the field of Lyme disease, defining the key molecules expressed by tick-borne spirochetes will move us one step closer toward understanding how this pathogen invades, disseminates and persists in the mammalian host. ..
  39. Donor Antigen-Induced Peripheral Tolerance
    Dianne McKay; Fiscal Year: 2006
    ..We believe that intracellular signaling alterations that lead to alloantigen-induced tolerance may provide novel targets for a new generation of tolerizing immunosuppressive agents. ..
  40. TLR4 as an LPS sendor and susceptibility locus
    Bruce Beutler; Fiscal Year: 2007
    ..Also known as Trif, or as Ticam-1, this adapter is essential for all MyD88-independentsignaling from both receptors, but does not transduce signals from the other TLRs...
  41. Immunological Basis for H. Pylori-Related Malignancies
    Marygorret Obonyo; Fiscal Year: 2006
    ..Under this award, the candidate will be able to develop this work into a productive project that will gain independent funding. ..
  42. TLR5 and Pulmonary Innate Immunity
    THOMAS HAWN; Fiscal Year: 2009
    ..The immunogenetic models derived from these studies will illuminate the molecular basis of why individuals have different susceptibility to flagellated bacterial infections and hopefully culminate in novel insights for future therapies. ..
  43. MECHANISMS OF DONOR SPLEEN INDUCED TRANSPLANT TOLERANCE
    Daniel Goldstein; Fiscal Year: 2004
    ..The career development program, mentor and didactic courses are designed to allow Dr. Goldstein to become an independent investigator by the end of the award period. ..
  44. MECHANISMS OF NOVEL ANTI-INFLAMMATORY ACTIONS OF SLPI
    Aihao Ding; Fiscal Year: 2007
    ..unreadable] [unreadable]..