Research Topics
Genomes and Genes | Peter MurraySummaryAffiliation: St. Jude Children's Research Hospital Country: USA Publications
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Publications
Restraint of inflammatory signaling by interdependent strata of negative regulatory pathwaysPeter J Murray
Department of Infectious Diseases and Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennessee, USA
Nat Immunol 13:916-24. 2012....
Increased antimycobacterial immunity in interleukin-10-deficient miceP J Murray
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, Tennessee 38105 2794, USA
Infect Immun 67:3087-95. 1999....- Obstacles and opportunities for understanding macrophage polarizationPeter J Murray
Department of Infectious Diseases, St Jude Children s Research Hospital, 262 Danny Thomas Pl, Memphis, TN 38105, USA
J Leukoc Biol 89:557-63. 2011..Here, we briefly summarize current features of macrophage polarization and discuss the roles of various macrophage subpopulations and macrophage-associated genes in health and disease... 
Gut Nod2 calls the bone marrow for monocyte reinforcementsPeter J Murray
Departments of Infectious Diseases and Immunology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
Immunity 34:693-5. 2011..In this issue of Immunity, Kim et al. (2011) demonstrate that Nod2 is responsible for regulating monocyte-attracting chemokines to the inflamed gut...- Understanding and exploiting the endogenous interleukin-10/STAT3-mediated anti-inflammatory responsePeter J Murray
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
Curr Opin Pharmacol 6:379-86. 2006..Nevertheless, the signaling pathway used by the IL-10 receptor to generate the anti-inflammatory response is only beginning to be understood and could be a way to regulate inflammation by pharmacological agents... - Macrophages as a battleground for toxoplasma pathogenesisPeter J Murray
Departments of Infectious Diseases and Immunology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
Cell Host Microbe 9:445-7. 2011..The results suggest that T. gondii and the ROP kinases can be used to probe immune signaling pathways... - The primary mechanism of the IL-10-regulated antiinflammatory response is to selectively inhibit transcriptionPeter J Murray
Department of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
Proc Natl Acad Sci U S A 102:8686-91. 2005.... - NOD proteins: an intracellular pathogen-recognition system or signal transduction modifiers?Peter J Murray
Department of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
Curr Opin Immunol 17:352-8. 2005..However, the idea of an intracellular system that specifically recognizes bacterial cell components is controversial and alternative functions of NODs are possible including regulating signal transduction systems... - The JAK-STAT signaling pathway: input and output integrationPeter J Murray
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38104, USA
J Immunol 178:2623-9. 2007..New data suggests that SOCS proteins introduce additional diversity into the JAK-STAT pathway by adjusting the output of activated STATs that alters downstream gene activation... - Protective and pathogenic functions of macrophage subsetsPeter J Murray
Department of Infectious Diseases, St Jude Children s Research Hospital, 262 Danny Thomas Place, Memphis, Tennessee 38105, USA
Nat Rev Immunol 11:723-37. 2011..Finally, we briefly discuss the characterization of macrophage heterogeneity in humans... - Defining the requirements for immunological control of mycobacterial infectionsP J Murray
Dept of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
Trends Microbiol 7:366-72. 1999..Latency - the seemingly quiescent phase of bacterial persistence - is the central problem in controlling tuberculosis and will be the next frontier of research... - STAT3-mediated anti-inflammatory signallingP J Murray
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
Biochem Soc Trans 34:1028-31. 2006..Understanding IL-10 signalling should be a gateway to the development of broadly acting anti-inflammatory agents... - Re-examination of the role of suppressor of cytokine signaling 1 (SOCS1) in the regulation of toll-like receptor signalingSebastien Gingras
Howard Hughes Medical Institute, Department of Biochemistry, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
J Biol Chem 279:54702-7. 2004..We conclude that previous reports linking SOCS1 to TLR signaling are most likely due to effects on IFN-alpha/beta receptor signaling... - Role of nod2 in the response of macrophages to toll-like receptor agonistsAnne Laure Pauleau
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
Mol Cell Biol 23:7531-9. 2003..These results argue that Nod2 does not play an essential, nonredundant role in the response of macrophages to bacterial products but rather plays unexpected roles in regulating systemic responses to pathogens... - SOCS3 regulates the plasticity of gp130 signalingRoland Lang
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
Nat Immunol 4:546-50. 2003..Thus, SOCS3 functions to control the quality of the response to IL-6 and prevents the activation of an IFN-induced program of gene expression... - Shaping gene expression in activated and resting primary macrophages by IL-10Roland Lang
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38015, USA
J Immunol 169:2253-63. 2002..For all genes examined, the effects of IL-10 were determined to be STAT3-dependent. These results suggest that IL-10 regulates STAT3-dependent pathways that selectively target a broad component of LPS-induced genes at the mRNA level... - The platelet activating factor receptor is not required for exacerbation of bacterial pneumonia following influenzaJonathan A McCullers
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, Tennessee 38105 2794, USA
Scand J Infect Dis 40:11-7. 2008.... - beta-Arrestin 1 participates in platelet-activating factor receptor-mediated endocytosis of Streptococcus pneumoniaeJana N Radin
Department of Infectious Diseases, St Jude Children s Research Hospital, Mailstop 320 IRC 8057, 332 N Lauderdale Rd, Memphis, TN 38105, USA
Infect Immun 73:7827-35. 2005..Overexpression of beta-arrestin in endothelial cells decreased colocalization with Rab7. We conclude that the association of beta-arrestin with the PAFr contributes to successful translocation of pneumococci... - The TLR2-MyD88-NOD2-RIPK2 signalling axis regulates a balanced pro-inflammatory and IL-10-mediated anti-inflammatory cytokine response to Gram-positive cell wallsLilian O Moreira
Department of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
Cell Microbiol 10:2067-77. 2008.... - Arginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signalingJoseph E Qualls
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
Sci Signal 3:ra62. 2010.... - Cutting edge: A transcriptional repressor and corepressor induced by the STAT3-regulated anti-inflammatory signaling pathwayKarim C El Kasmi
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
J Immunol 179:7215-9. 2007..Collectively our data suggest that ETV3 and SBNO2 are components of the pathways that contribute to the downstream anti-inflammatory effects of IL-10... - General nature of the STAT3-activated anti-inflammatory responseKarim C El Kasmi
Department of Infectious Diseases, St Jude s Children s Research Hospital, Memphis, TN 38105, USA
J Immunol 177:7880-8. 2006..We conclude that the AIR is a generic cytokine signaling pathway dependent on STAT3 but not unique to the IL-10R... - Platelet-activating factor receptor and innate immunity: uptake of gram-positive bacterial cell wall into host cells and cell-specific pathophysiologySophie Fillon
Department of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA
J Immunol 177:6182-91. 2006..Thus, PAFr shepherds phosphorylcholine-containing bacterial components such as the cell wall into host cells from where the response ranges from quiescence to severe pathophysiology... - LAG-3 regulates plasmacytoid dendritic cell homeostasisCreg J Workman
Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
J Immunol 182:1885-91. 2009..Collectively, our data suggests that LAG-3 plays an important but selective cell intrinsic and cell extrinsic role in pDC biology, and may serve as a key functional marker for their study... - WASP- mice exhibit defective immune responses to influenza A virus, Streptococcus pneumoniae, and Mycobacterium bovis BCGSamita Andreansky
Department of Immunology, St Jude Children s Hospital, Memphis, TN 38104, USA
Exp Hematol 33:443-51. 2005..To quantify the immune response of WASP- mice to three different pathogens: influenza A virus, Streptococcus pneumoniae, and Mycobacterium bovis... - Autocrine deactivation of macrophages in transgenic mice constitutively overexpressing IL-10 under control of the human CD68 promoterRoland Lang
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
J Immunol 168:3402-11. 2002.... - Cell wall-mediated neuronal damage in early sepsisCarlos J Orihuela
Infectious Diseases, St. Jude Children's Research Hospital, Mailstop 320 IRC 8057, 332 N. Lauderdale Rd, Memphis, TN 38105, USA
Infect Immun 74:3783-9. 2006..Thus, cell wall drives SAND through IL-10-repressible inflammatory events. Treatment with CDP-choline ameliorated SAND, suggesting that it may be an effective adjunctive therapy to increase survival and reduce organ damage in sepsis... - Toll-like receptor-induced arginase 1 in macrophages thwarts effective immunity against intracellular pathogensKarim C El Kasmi
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, Tennessee 38015, USA
Nat Immunol 9:1399-406. 2008..Specific elimination of Arg1 in macrophages favored host survival during T. gondii infection and decreased lung bacterial load during tuberculosis infection... - Conditional knockout mice reveal distinct functions for the global transcriptional coactivators CBP and p300 in T-cell developmentLawryn H Kasper
Department of Biochemistry, St Jude Children s Research Hospital, 332 N Lauderdale, Memphis, TN 38105, USA
Mol Cell Biol 26:789-809. 2006..Thus, CBP and p300 each supply a surprising degree of redundant coactivation capacity in T cells and macrophages, although each gene has also unique properties in thymocyte development... - Enhancer-mediated control of macrophage-specific arginase I expressionAnne Laure Pauleau
Department of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
J Immunol 172:7565-73. 2004..Identification of a powerful extrahepatic regulatory enhancer for arginase I provides potential to manipulate arginase I activity in immune cells while sparing liver urea cycle function... - Modulation of adaptive immunity by different adjuvant-antigen combinations in mice lacking Nod2Lilian O Moreira
Department of Infectious Diseases, St Jude Children s Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA
Vaccine 26:5808-13. 2008..Collectively, our results argue that oil emulsions deserve greater attention for their immunostimulatory properties... - Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survivalMohamed Lamkanfi
Department of Immunology, St Jude Children s Research Hospital, Memphis, TN 38105 2794, USA
Blood 113:2742-5. 2009..These results reveal for the first time a nonredundant role for caspase-7 in vivo and identify caspase-7 inhibition as a component of the mechanism by which caspase inhibitors protect from endotoxin-induced mortality... - Nucleotide binding oligomerization domain 2 deficiency leads to dysregulated TLR2 signaling and induction of antigen-specific colitisTomohiro Watanabe
Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 CRC, Room 5W3940, 10 Center Drive, Bethesda, Maryland 20892, USA
Immunity 25:473-85. 2006..Thus, NOD2-deficient mice become susceptible to colitis as a result of increased TLR2 responses when they have the capacity to respond to an antigen expressed by mucosal bacteria... - Abrogation of anti-retinal autoimmunity in IL-10 transgenic mice due to reduced T cell priming and inhibition of disease effector mechanismsRajeev K Agarwal
The Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 180:5423-9. 2008.... - IL-10-independent STAT3 activation by Toxoplasma gondii mediates suppression of IL-12 and TNF-alpha in host macrophagesBarbara A Butcher
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
J Immunol 174:3148-52. 2005..gondii exploits host STAT3 to prevent LPS-triggered IL-12 and TNF-alpha production, revealing for the first time a molecular mechanism underlying the parasite's suppressive effect on macrophage proinflammatory cytokine production... - IFN regulatory factor 3-dependent induction of type I IFNs by intracellular bacteria is mediated by a TLR- and Nod2-independent mechanismSilvia Stockinger
Max F Perutz Laboratories, University Department at the Vienna Biocenter, Department of Microbiology and Genetics, University of Vienna, Austria
J Immunol 173:7416-25. 2004..monocytogenes stimulates a novel TLR- and Nod2-independent pathway to target IRF3 and the type I IFN genes... - NOD2 is a negative regulator of Toll-like receptor 2-mediated T helper type 1 responsesTomohiro Watanabe
Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 Room 11N238, 10 Center Drive, Bethesda, Maryland 20892, USA
Nat Immunol 5:800-8. 2004..Thus, CARD15 mutations may lead to disease by causing excessive T(H)1 responses... - Cytokine signaling modules in inflammatory responsesJOHN J O'SHEA
Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20852, USA
Immunity 28:477-87. 2008.... - Control of dual-specificity phosphatase-1 expression in activated macrophages by IL-10Michael Hammer
Institute of Medical Microbiology, Immunology and Hygiene, Technical University Munich, Munich, Germany
Eur J Immunol 35:2991-3001. 2005..Thus, these data suggest an operational link between IL-10 and inhibition of p38 MAPK via sustained expression of DUSP1... - IL-10 suppresses mast cell IgE receptor expression and signaling in vitro and in vivoSarah Kennedy Norton
Department of Biology, Virginia Commonwealth University, Richmond, VA 23284, USA
J Immunol 180:2848-54. 2008..IL-10 may hence serve as a mediator of mast cell homeostasis, preventing excessive activation and the development of chronic inflammation... - Persistent Coxiella burnetii infection in mice overexpressing IL-10: an efficient model for chronic Q fever pathogenesisSoraya Meghari
Unite des Rickettsies, CNRS UMR 6020, Institut Federatif de Recherche 48, Universite de la Mediterranee, Faculte de Medecine, Marseille, France
PLoS Pathog 4:e23. 2008..To our knowledge, this is the first efficient model for chronic Q fever pathogenesis... - Muramyl dipeptide activation of nucleotide-binding oligomerization domain 2 protects mice from experimental colitisTomohiro Watanabe
Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland 20892, USA
J Clin Invest 118:545-59. 2008.... - Hypervirulent M. tuberculosis W/Beijing strains upregulate type I IFNs and increase expression of negative regulators of the Jak-Stat pathwayClaudia Manca
Laboratory of Mycobacterial Immunity and Pathogenesis, Public Health Research Institute, International Center for Public Health, 225 Warren Street, Newark, NJ 07103-3535, USA
J Interferon Cytokine Res 25:694-701. 2005..Taken together, these results suggest that increased type I IFNs may be deleterious for survival of M. tuberculosis-infected mice in association with reduced Th1 immunity... - Induction of suppressor of cytokine signaling-1 by Toxoplasma gondii contributes to immune evasion in macrophages by blocking IFN-gamma signalingStefan Zimmermann
Institute of Medical Microbiology and Hygiene, Philipps University, Marburg, Germany
J Immunol 176:1840-7. 2006..gondii on IFN-gamma were diminished in macrophages from SOCS-1-/- mice. The results suggest that induction of SOCS proteins within phagocytes due to infection with T. gondii contributes to the parasite's immune evasion strategies... - Interleukin-10 induces apoptosis in developing mast cells and macrophagesDaniel P Bailey
Department of Biology, Virginia Commonwealth University, Richmond, 23284 2012, USA
J Leukoc Biol 80:581-9. 2006..The ability of IL-10 to inhibit survival could support immune homeostasis by dampening inflammatory responses and preventing chronic inflammation... - Nucleotide-binding oligomerization domain protein 2-deficient mice control infection with Mycobacterium tuberculosisSheetal Gandotra
Department of Microbiology and Immunology, Weill Cornell Medical College, Box 62, 1300 York Avenue, New York, NY 10021, USA
Infect Immun 75:5127-34. 2007..tuberculosis infection. Thus, NOD2 appears to participate in the recognition of M. tuberculosis by antigen-presenting cells in vitro yet is dispensable for the control of the pathogen during in vivo infection... - Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammationDivya Vats
Division of Endocrinology, Metabolism and Gerontology, Department of Medicine and Graduate Program in Immunology, Stanford University School of Medicine, Stanford, California 94305, USA
Cell Metab 4:13-24. 2006.... - Targeting vector construction by yeast artificial chromosome modificationPeter J Murray
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, USA
Methods Mol Biol 349:127-37. 2006..This chapter describes a simple procedure where YACs can be modified to produce targeting vectors of various sizes... - Signalling pathways and molecular interactions of NOD1 and NOD2Warren Strober
Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 CRC, 5W3940, 10 Center Drive, Bethesda, Maryland 20892, USA
Nat Rev Immunol 6:9-20. 2006.... - STAT3 governs distinct pathways in emergency granulopoiesis and mature neutrophilsAthanasia D Panopoulos
Department of Immunology, The University of Texas M D Anderson Cancer Center, PO Box 301402, Unit 902, Houston, TX 77030 1903, USA
Blood 108:3682-90. 2006..Our results demonstrate the existence of distinct STAT3 target pathways in neutrophils required for granulopoiesis and innate immunity...
Research Grants
- Role of SOCS proteins in host-pathogen responsesPeter Murray; Fiscal Year: 2003..PERFORMANCE SITE (S) (organization, city, state) St. Jude Children's Research Hospital, Memphis, TN . ..
- Role of Macrophage Arginase in Anti-Bacterial ImmunityPeter Murray; Fiscal Year: 2009..The outcomes of the proposed studies will reveal new elements of Arg I function and provide rationale for approaching Arg I as a target in inflammatory diseases. ..