tumor necrosis factors

Summary

Summary: A family of proteins that were originally identified by their ability to cause NECROSIS of NEOPLASMS. Their necrotic effect on cells is mediated through TUMOR NECROSIS FACTOR RECEPTORS which induce APOPTOSIS.

Top Publications

  1. ncbi TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity
    Patrick J Donohue
    Department of Vascular Biology, Jerome H Holland Laboratory for the Biomedical Sciences, American Red Cross, 15601 Crabbs Branch Way, Rockville, MD 20855, USA
    Arterioscler Thromb Vasc Biol 23:594-600. 2003
  2. ncbi TWEAK/Fn14 pathway: an immunological switch for shaping tissue responses
    Linda C Burkly
    Immunology Discovery Research, Biogen Idec, Inc, Cambridge, MA 02142, USA
    Immunol Rev 244:99-114. 2011
  3. ncbi TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis
    Y Chicheportiche
    Department of Pathology, University of Geneva, 1211 Geneva 4, Switzerland
    J Biol Chem 272:32401-10. 1997
  4. pmc C1q/TNF-related protein-3 (CTRP3), a novel adipokine that regulates hepatic glucose output
    Jonathan M Peterson
    Department of Physiology and Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Biol Chem 285:39691-701. 2010
  5. ncbi OX40 promotes Bcl-xL and Bcl-2 expression and is essential for long-term survival of CD4 T cells
    P R Rogers
    Division of Immunochemistry, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA
    Immunity 15:445-55. 2001
  6. ncbi TWEAK is expressed by glial cells, induces astrocyte proliferation and increases EAE severity
    Sophie Desplat-Jego
    NICN CNRS FRE 2533, IFR Jean Roche, Universite de la Mediterranee, 13 916 Cedex 20, Marseilles, France
    J Neuroimmunol 133:116-23. 2002
  7. pmc The human Fn14 receptor gene is up-regulated in migrating glioma cells in vitro and overexpressed in advanced glial tumors
    Nhan L Tran
    Neuro Oncology Research, Barrow Neurological Institute, Phoenix, Arizona, USA
    Am J Pathol 162:1313-21. 2003
  8. pmc Soluble TWEAK plasma levels as a novel biomarker of endothelial function in patients with chronic kidney disease
    Mahmut Ilker Yilmaz
    Department of Nephrology, Gulhane School of Medicine, Ankara, Turkey
    Clin J Am Soc Nephrol 4:1716-23. 2009
  9. ncbi TWEAK induces angiogenesis and proliferation of endothelial cells
    C N Lynch
    Abbott Laboratories, Abbott Park, Illinois 60064, USA
    J Biol Chem 274:8455-9. 1999
  10. ncbi A novel TNF receptor family member binds TWEAK and is implicated in angiogenesis
    S R Wiley
    Immunex Corporation, 51 University Street, Seattle, WA 98101, USA
    Immunity 15:837-46. 2001

Research Grants

  1. FUNCTIONAL ROLE OF TNF-ALPHA CYTOKINES IN BONE REPAIR
    Louis Gerstenfeld; Fiscal Year: 2004
  2. Design of Biocompatible NiTi (Nitinol) Surfaces
    PATRICIA THIEL; Fiscal Year: 2002
  3. VITAMIN D COMPOUNDS FOR INFLAMMATORY BOWEL DISEASE
    COLLEEN HAYES; Fiscal Year: 1999
  4. TNFR Members in T Cell Immunity to Vaccinia
    Michael Croft; Fiscal Year: 2010
  5. The Role of 4-1BB in T Cell and APC Interactions
    Michael Croft; Fiscal Year: 2010
  6. Transport of TNFalpha across the BBB
    Weihong Pan; Fiscal Year: 2008
  7. Transport of neurotrophic cytokines after spinal cord injury
    Weihong Pan; Fiscal Year: 2007
  8. Role of TWEAK and Fn14 in Vascular Biology
    JEFFREY WINKLES; Fiscal Year: 2005
  9. The Fn14 Receptor and Brain Tumor Invasion
    Jeffrey A Winkles; Fiscal Year: 2011
  10. Vaccines to Generate Neutralizing Anti-HIV Antibodies
    RICHARD KORNBLUTH; Fiscal Year: 2008

Detail Information

Publications279 found, 100 shown here

  1. ncbi TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity
    Patrick J Donohue
    Department of Vascular Biology, Jerome H Holland Laboratory for the Biomedical Sciences, American Red Cross, 15601 Crabbs Branch Way, Rockville, MD 20855, USA
    Arterioscler Thromb Vasc Biol 23:594-600. 2003
    ..We also determined whether a soluble Fn14-Fc fusion protein could inhibit TWEAK biologic activity on ECs and investigated TWEAK signal transduction in ECs...
  2. ncbi TWEAK/Fn14 pathway: an immunological switch for shaping tissue responses
    Linda C Burkly
    Immunology Discovery Research, Biogen Idec, Inc, Cambridge, MA 02142, USA
    Immunol Rev 244:99-114. 2011
    ..Whereas transient TWEAK/Fn14 activation promotes productive tissue responses after injury, excessive or persistent TWEAK/Fn14 activation drives pathological tissue responses, leading to progressive damage and degeneration...
  3. ncbi TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis
    Y Chicheportiche
    Department of Pathology, University of Geneva, 1211 Geneva 4, Switzerland
    J Biol Chem 272:32401-10. 1997
    ....
  4. pmc C1q/TNF-related protein-3 (CTRP3), a novel adipokine that regulates hepatic glucose output
    Jonathan M Peterson
    Department of Physiology and Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Biol Chem 285:39691-701. 2010
    ..This study provides the first functional evidence linking CTRP3 to hepatic glucose metabolism and establishes CTRP3 as a novel adipokine...
  5. ncbi OX40 promotes Bcl-xL and Bcl-2 expression and is essential for long-term survival of CD4 T cells
    P R Rogers
    Division of Immunochemistry, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA
    Immunity 15:445-55. 2001
    ..Moreover, retroviral transduction of OX40-/- T cells with Bcl-xL or Bcl-2 reverses their survival defect. Thus, a temporal relationship exists between CD28 and OX40, with OX40 being a critical regulator of antigen-driven T cell survival...
  6. ncbi TWEAK is expressed by glial cells, induces astrocyte proliferation and increases EAE severity
    Sophie Desplat-Jego
    NICN CNRS FRE 2533, IFR Jean Roche, Universite de la Mediterranee, 13 916 Cedex 20, Marseilles, France
    J Neuroimmunol 133:116-23. 2002
    ..Finally, EAE severity is enhanced in soluble TWEAK-overexpressing transgenic mice. These results support the contention that TWEAK is involved in CNS inflammation...
  7. pmc The human Fn14 receptor gene is up-regulated in migrating glioma cells in vitro and overexpressed in advanced glial tumors
    Nhan L Tran
    Neuro Oncology Research, Barrow Neurological Institute, Phoenix, Arizona, USA
    Am J Pathol 162:1313-21. 2003
    ..These results suggest a positive role for TWEAK and Fn14 in glioma progression and indicate that Fn14 gene expression may serve as a marker for invasive glioma cells...
  8. pmc Soluble TWEAK plasma levels as a novel biomarker of endothelial function in patients with chronic kidney disease
    Mahmut Ilker Yilmaz
    Department of Nephrology, Gulhane School of Medicine, Ankara, Turkey
    Clin J Am Soc Nephrol 4:1716-23. 2009
    ....
  9. ncbi TWEAK induces angiogenesis and proliferation of endothelial cells
    C N Lynch
    Abbott Laboratories, Abbott Park, Illinois 60064, USA
    J Biol Chem 274:8455-9. 1999
    ..Pellets containing TWEAK induce a strong angiogenic response when implanted in rat corneas, suggesting a role for TWEAK in vasculature formation in vivo...
  10. ncbi A novel TNF receptor family member binds TWEAK and is implicated in angiogenesis
    S R Wiley
    Immunex Corporation, 51 University Street, Seattle, WA 98101, USA
    Immunity 15:837-46. 2001
    ..Soluble TweakR inhibits endothelial cell migration in vitro and corneal angiogenesis in vivo...
  11. pmc TWEAK induces liver progenitor cell proliferation
    Aniela Jakubowski
    Department of Exploratory Science, Biogen Idec Inc, Cambridge, Massachusetts 02142, USA
    J Clin Invest 115:2330-40. 2005
    ..We conclude that TWEAK has a selective mitogenic effect for liver oval cells that distinguishes it from other previously described growth factors...
  12. ncbi TWEAK/Fn14 pathway: a nonredundant role in intestinal damage in mice through a TWEAK/intestinal epithelial cell axis
    Taeko Dohi
    Department of Gastroenterology, Research Institute, International Medical Center of Japan, Tokyo, Japan
    Gastroenterology 136:912-23. 2009
    ..The role of this pathway in the intestine has not been previously reported...
  13. ncbi Impact of soluble TWEAK and CD163/TWEAK ratio on long-term cardiovascular mortality in patients with peripheral arterial disease
    Grazina Urbonaviciene
    Vascular Research Unit, Department of Vascular Surgery, Viborg Hospital, Heibergs Alle 4, DK 8800 Viborg, Denmark
    Atherosclerosis 219:892-9. 2011
    ..We examined the associations between sTWEAK, its scavenger receptor sCD163, sCD163/sTWEAK ratio and risk for long-term all-cause and cardiovascular mortality in patients with lower-extremity peripheral arterial disease (PAD)...
  14. pmc TNF-like weak inducer of apoptosis (TWEAK) activates proinflammatory signaling pathways and gene expression through the activation of TGF-beta-activated kinase 1
    Mukesh Kumar
    Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY 40202, USA
    J Immunol 182:2439-48. 2009
    ..Collectively, our study demonstrates that TAK1 and Akt are the important components of TWEAK-induced proinflammatory signaling and gene expression...
  15. ncbi C1q/TNF-related protein-3 represents a novel and endogenous lipopolysaccharide antagonist of the adipose tissue
    Andrea Kopp
    Department of Internal Medicine I, University of Regensburg, D 93042 Regensburg, Germany
    Endocrinology 151:5267-78. 2010
    ..CTRP-3 inhibits three basic and common proinflammatory pathways involved in obesity and type 2 diabetes mellitus (adipo-inflammation) by acting as an endogenous LPS antagonist of the adipose tissue...
  16. ncbi Dual role for TWEAK in angiogenic regulation
    Aniela Jakubowski
    Department of Exploratory Science, Biogen Inc, 12 Cambridge Center, Cambridge, Massachusetts 02142, USA
    J Cell Sci 115:267-74. 2002
    ..Thus, our observations suggest that TWEAK may differentially regulate microvascular growth, remodeling and/or maintenance in vivo, depending upon the angiogenic context...
  17. ncbi TWEAK, a member of the TNF superfamily, is a multifunctional cytokine that binds the TweakR/Fn14 receptor
    Steven R Wiley
    Amgen Corporation, Seattle, WA 98101, USA
    Cytokine Growth Factor Rev 14:241-9. 2003
    ..Although these studies have contributed a significant amount of new information, numerous questions still remain regarding the role of TWEAK in both normal physiology and the pathogenesis of human disease...
  18. ncbi TWEAK is a positive regulator of cardiomyocyte proliferation
    Tatyana Novoyatleva
    Department of Cardiac Development and Remodelling, Excellence Cluster Cardio Pulmonary System, Max Planck Institute for Heart and Lung Research, Parkstrasse 1, Bad Nauheim 61231, Germany
    Cardiovasc Res 85:681-90. 2010
    ..Here, we determine the effect of TNF-related weak inducer of apoptosis (TWEAK) on cardiomyocytes, a cytokine known to regulate proliferation in several other cell types...
  19. ncbi Identification of soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) as a possible biomarker of subclinical atherosclerosis
    Luis M Blanco-Colio
    Vascular Research Laboratory, Fundacion Jimenez Diaz, Autonoma University, 28040, Madrid, Spain
    Arterioscler Thromb Vasc Biol 27:916-22. 2007
    ..Our aim was to identify proteins differentially released by healthy versus atherosclerotic arterial walls, which could be found in plasma and serve as markers of atherosclerosis...
  20. pmc The cytokine tumor necrosis factor-like weak inducer of apoptosis and its receptor fibroblast growth factor-inducible 14 have a neuroprotective effect in the central nervous system
    Ramiro Echeverry
    Department of Neurology and Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, GA, USA
    J Neuroinflammation 9:45. 2012
    ..Accordingly, in this work we tested the hypothesis that the interaction between TWEAK and Fn14 induces tolerance to lethal hypoxic and ischemic conditions...
  21. pmc Studies of binding of tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) to fibroblast growth factor inducible 14 (Fn14)
    Andrea Fick
    Division of Molecular Internal Medicine, Department of Internal Medicine II, University Hospital Wurzburg, Rontgenring 11, 97070 Wurzburg, Germany
    J Biol Chem 287:484-95. 2012
    ..Thus, although ∼25 activated TNFR1 trimers were sufficient to trigger half-maximal IL8 production, more than 2500 cell-bound oligomerized TWEAK trimers were required to elicit a similar response...
  22. pmc The Fn14 cytoplasmic tail binds tumour-necrosis-factor-receptor-associated factors 1, 2, 3 and 5 and mediates nuclear factor-kappaB activation
    Sharron A N Brown
    Vascular Biology Department, Jerome H Holland Laboratory for the Biomedical Sciences, American Red Cross, 15601 Crabbs Branch Way, Rockville, MD 20855, USA
    Biochem J 371:395-403. 2003
    ..These results indicate that Fn14 is a functional TWEAK receptor that can associate with four distinct TRAF family members and stimulate the NF-kappaB transcription factor signalling pathway...
  23. ncbi Tumor necrosis factor-like weak inducer of apoptosis-induced neurodegeneration
    Ioana Potrovita
    Department of Neurology, University of Heidelberg, D 69120 Heidelberg, Germany
    J Neurosci 24:8237-44. 2004
    ..In summary, our data show that TWEAK induces neuronal cell death and is involved in neurodegeneration in vivo...
  24. ncbi Role of TWEAK and Fn14 in tumor biology
    Jeffrey A Winkles
    Department of Surgery, Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    Front Biosci 12:2761-71. 2007
    ..In this paper, we first summarize the general properties of these two proteins and then review the available data implicating TWEAK and Fn14 in multiple aspects of tumor biology...
  25. pmc Genetic ablation of TWEAK augments regeneration and post-injury growth of skeletal muscle in mice
    Ashwani Mittal
    Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA
    Am J Pathol 177:1732-42. 2010
    ..Collectively, our study suggests that TWEAK negatively regulates muscle regeneration and that TWEAK is a potential therapeutic target to enhance skeletal muscle regeneration in vivo...
  26. ncbi TWEAK attenuates the transition from innate to adaptive immunity
    Heather Maecker
    Department of Molecular Oncology, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    Cell 123:931-44. 2005
    ..Thus, TWEAK suppresses production of IFN-gamma and IL-12, curtailing the innate response and its transition to adaptive TH1 immunity...
  27. pmc A novel role for tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in the development of cardiac dysfunction and failure
    Mohit Jain
    Division of Cardiology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Circulation 119:2058-68. 2009
    ..Although many of the processes and downstream signals regulated by the TWEAK/Fn14 pathway have been implicated in the development of cardiac dysfunction, the role of TWEAK in the cardiovascular system is completely unknown...
  28. ncbi TWEAKing tissue remodeling by a multifunctional cytokine: role of TWEAK/Fn14 pathway in health and disease
    Linda C Burkly
    Department of Immunobiology, Biogen Idec, 12 Cambridge Center, Cambridge, MA 02142, USA
    Cytokine 40:1-16. 2007
    ..In addition to a perspective of the biology, we discuss potential therapeutic strategies targeting this pathway for the treatment of tissue injury, chronic inflammatory diseases and cancer...
  29. pmc Tumor necrosis factor-related weak inducer of apoptosis augments matrix metalloproteinase 9 (MMP-9) production in skeletal muscle through the activation of nuclear factor-kappaB-inducing kinase and p38 mitogen-activated protein kinase: a potential role of
    Hong Li
    Departments of Anatomical Sciences and Neurobiology and Physiology and Biophysics, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA
    J Biol Chem 284:4439-50. 2009
    ..The study unveils a novel mechanism of skeletal muscle tissue destruction in pathological conditions...
  30. ncbi GITR/GITRL: more than an effector T cell co-stimulatory system
    Giuseppe Nocentini
    Dipartimento di Medicina Clinica e Sperimentale, Sezione di Farmacologia, Tossicologia e Chemioterapia, Universita di Perugia, Perugia, Italy
    Eur J Immunol 37:1165-9. 2007
    ..This review summarizes recent results about the GITR/GITRL system, focusing on the interplay between APC, effector and regulatory T cells...
  31. ncbi Pro-inflammatory effect of TWEAK/Fn14 interaction on human umbilical vein endothelial cells
    Norihiro Harada
    Department of Immunology, Juntendo University School of Medicine, 2 1 1 Hongo, Bunkyo ku, Tokyo, Japan
    Biochem Biophys Res Commun 299:488-93. 2002
    ..These results indicated that TWEAK could induce pro-inflammatory reactions via Fn14 on HUVEC...
  32. ncbi Soluble tumor necrosis factor-like weak inducer of apoptosis overexpression in HEK293 cells promotes tumor growth and angiogenesis in athymic nude mice
    David H Ho
    Department of Surgery and Physiology and the University of Maryland Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, USA
    Cancer Res 64:8968-72. 2004
    ..This result suggests that the TWEAK-Fn14 signaling system may be a potential regulator of human tumorigenesis...
  33. ncbi Fibroblast growth factor-inducible 14 mediates multiple pathways of TWEAK-induced cell death
    Masafumi Nakayama
    Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan
    J Immunol 170:341-8. 2003
    ..These results revealed that the multiple pathways of TWEAK-induced cell death are solely mediated by Fn14...
  34. pmc CD4 T cell cytokine differentiation: the B cell activation molecule, OX40 ligand, instructs CD4 T cells to express interleukin 4 and upregulates expression of the chemokine receptor, Blr-1
    S Flynn
    Department of Immunology, Birmingham Medical School, Birmingham B15 2TT, United Kingdom
    J Exp Med 188:297-304. 1998
    ..Our data suggest that OX40L on antigen-activated B cells instructs naive T cells to differentiate into Th2 cells and migrate into B follicles, where T cell-dependent germinal centers develop...
  35. ncbi TWEAK mediates signal transduction and differentiation of RAW264.7 cells in the absence of Fn14/TweakR. Evidence for a second TWEAK receptor
    Tara C Polek
    Department of Bioimmunotherapy, Section of Cytokine Research, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA
    J Biol Chem 278:32317-23. 2003
    ..We propose that the biological effects of TWEAK are mediated by binding to one of at least two distinct receptors that induce differential activation of downstream signaling pathways...
  36. ncbi Circulating sTWEAK improves the prediction of coronary artery disease
    Zorana Jelic-Ivanovic
    Institute of Medical Biochemistry, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia
    Clin Biochem 42:1381-6. 2009
    ..Decreased concentrations of circulating soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) were recently reported to be associated with atherosclerosis, but there are still no data concerning its predictive performance...
  37. ncbi Multiple members of the TNF superfamily contribute to IFN-gamma-mediated inhibition of erythropoiesis
    Nadia Felli
    Department of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanita, Rome, Italy
    J Immunol 175:1464-72. 2005
    ....
  38. ncbi Functional expression of TWEAK in human hepatocellular carcinoma: possible implication in cell proliferation and tumor angiogenesis
    Tomoyuki Kawakita
    First Department of Internal Medicine, Mie University School of Medicine, Tsu, Mie 514 8507, Japan
    Biochem Biophys Res Commun 318:726-33. 2004
    ..In conclusion, these results indicate that TWEAK might play a critical role in HCC cellular proliferation using both autocrine and paracrine mechanisms, and modulate tumor-related angiogenesis...
  39. ncbi TWEAK is expressed at the cell surface of monocytes during multiple sclerosis
    Sophie Desplat-Jego
    Neurobioligie des Interactions Cellulaires et Neurophysiopathologie, CNRS UMR 6184, IFR Jean Roche, 51 Bd Pierre Dramard, 13 916 Marseille cedex 20, France
    J Leukoc Biol 85:132-5. 2009
    ..We demonstrated for the first time that TWEAK is expressed at the cell surface of monocytes during MS, especially in the CISSMS group. Our results support the proposal that TWEAK could be a target for antibody therapy in MS...
  40. ncbi Tumour necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor Fn14 during cardiac remodelling in rats
    E Mustonen
    Department of Pharmacology and Toxicology, Institute of Biomedicine, Biocenter Oulu, Oulu, Finland
    Acta Physiol (Oxf) 199:11-22. 2010
    ..We examined the concomitant tumour necrosis factor-like weak inducer of apoptosis (TWEAK)/Fn14 expression in myocytes in vitro as well as in vivo in cardiac remodelling...
  41. ncbi Contribution of OX40/OX40 ligand interaction to the pathogenesis of rheumatoid arthritis
    T Yoshioka
    Department of Joint Disease and Rheumatism, Nippon Medical School, Tokyo, Japan
    Eur J Immunol 30:2815-23. 2000
    ..These results indicate that OX40/OX40L interaction may play a critical role in the development of RA...
  42. ncbi TWEAK-Fn14 pathway inhibition protects the integrity of the neurovascular unit during cerebral ischemia
    Xiaohui Zhang
    Department of Neurology and Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, GA 30322, USA
    J Cereb Blood Flow Metab 27:534-44. 2007
    ..These findings show that the cytokine TWEAK plays a role in the disruption of the structure of the NVU during cerebral ischemia and that TWEAK antagonism is a potential therapeutic strategy for acute cerebral ischemia...
  43. pmc Role of TL1A and its receptor DR3 in two models of chronic murine ileitis
    Giorgos Bamias
    Digestive Health Center of Excellence, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA
    Proc Natl Acad Sci U S A 103:8441-6. 2006
    ..Blockade of the TL1A/DR3 pathway may, therefore, offer therapeutic opportunities in Crohn's disease...
  44. ncbi Multiple pathways of TWEAK-induced cell death
    Masafumi Nakayama
    Department of Immunology, Allergy Research Center, Division of Pathology, Central Laboratory of Medical Sciences, Juntendo University School of Medicine, Tokyo, Japan
    J Immunol 168:734-43. 2002
    ..These results indicated that TWEAK could induce multiple pathways of cell death, including both caspase-dependent apoptosis and cathepsin B-dependent necrosis, in a cell type-specific manner via TWEAK receptor(s) distinct from DR3...
  45. ncbi Blocking OX-40/OX-40 ligand interaction in vitro and in vivo leads to decreased T cell function and amelioration of experimental allergic encephalomyelitis
    A D Weinberg
    Earle A Chiles Research Institute, Robert W Franz Cancer Research Center, Providence Portland Medical Center, Portland, OR 97213, USA
    J Immunol 162:1818-26. 1999
    ..Furthermore, the data suggest that agents designed to inhibit the OX-40L/OX-40R complex may be useful for treating autoimmune disease...
  46. ncbi New components of the necroptotic pathway
    Zhenru Zhou
    State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University, Xiamen, China
    Protein Cell 3:811-7. 2012
    ..Here we review the new members of this necroptosis pathway, MLKL, PGAM5, Drp1 and DAI, and discuss some of their possible applications according to recent findings...
  47. ncbi TWEAK-Fn14 interaction enhances plasminogen activator inhibitor 1 and tissue factor expression in atherosclerotic plaques and in cultured vascular smooth muscle cells
    Begona Munoz-Garcia
    Renal and Vascular Research Laboratory, Instituto de Investigacion Sanitaria, Fundacion Jimenez Diaz, Autonoma University, Avd Reyes Católicos 2, 28040 Madrid, Spain
    Cardiovasc Res 89:225-33. 2011
    ..However, the role of the TWEAK-Fn14 axis in thrombosis has not been previously investigated...
  48. ncbi Direct targeting of fibroblast growth factor-inducible 14 protein protects against renal ischemia reperfusion injury
    Kiyohiko Hotta
    Department of Surgery, Nara Medical University, Nara, Japan
    Kidney Int 79:179-88. 2011
    ..Thus, we conclude that Fn14 is a critical mediator in the pathogenesis of ischemia reperfusion injury...
  49. ncbi Origin and evolution of TNF and TNF receptor superfamilies
    Gregory D Wiens
    USDA ARS, National Center for Cool and Cold Water Aquaculture, Kearneysville, WV 25430, USA
    Dev Comp Immunol 35:1324-35. 2011
    ..The increasing interest and use of TNFSF and TNFRSF modulators in human and animal medicine underscores the need to understand the evolutionary origins as well as conserved and novel functions of these biologically important molecules...
  50. ncbi Mechanism of signal transduction in tumor necrosis factor-like weak inducer of apoptosis-induced matrix degradation by MMP-3 upregulation in disc tissues
    Masanori Wako
    Department of Orthopaedic Surgery, Graduate School of Medicine and Engineering, University of Yamanashi, Yamanashi, Japan
    Spine (Phila Pa 1976) 33:2489-94. 2008
    ..Molecular biologic and immuno-histologic analyses using in vitro murine intervertebral disc tissue culture...
  51. ncbi The adiponectin paralog CORS-26 has anti-inflammatory properties and is produced by human monocytic cells
    Johanna Weigert
    Department of Internal Medicine I, University of Regensburg, Germany
    FEBS Lett 579:5565-70. 2005
    ..Therefore CORS-26 may provide a new target for pharmacological drugs in inflammatory diseases like the metabolic syndrome...
  52. pmc Pharmacological modulation of GITRL/GITR system: therapeutic perspectives
    Giuseppe Nocentini
    Department of Clinical and Experimental Medicine, University of Perugia, Perugia, Italy
    Br J Pharmacol 165:2089-99. 2012
    ..However, differences between mouse and human GITRL/GITR systems suggest that further preclinical studies are needed to better understand how safe therapeutic results can be obtained and to design appropriate clinical trials...
  53. pmc Full-length, membrane-anchored TWEAK can function as a juxtacrine signaling molecule and activate the NF-kappaB pathway
    Sharron A N Brown
    Department of Surgery and Physiology, Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    J Biol Chem 285:17432-41. 2010
    ..Thus, TWEAK can act in a juxtacrine manner to initiate cellular responses, and this property may be important for TWEAK function during physiological wound repair and disease pathogenesis...
  54. ncbi Expression of TWEAK and its receptor Fn14 in the multiple sclerosis brain: implications for inflammatory tissue injury
    Barbara Serafini
    Department of Cell Biology and Neuroscience, Istituto Superiore di Sanita, Rome, Italy
    J Neuropathol Exp Neurol 67:1137-48. 2008
    ..Taken together, these findings indicate that the TWEAK/Fn14 pathway contributes to inflammation and tissue injury and is, therefore, a potential therapeutic target in MS...
  55. ncbi Studies on the interaction between TWEAK and the death receptor WSL-1/TRAMP (DR3)
    A Kaptein
    Cell Biology Department, GlaxoWellcome Medicines Research Centre, Stevenage, UK
    FEBS Lett 485:135-41. 2000
    ..Finally, cells isolated from WSL-1/TRAMP knockout mice are shown to retain their ability to interact with TWEAK. These results suggest that WSL-1/TRAMP is not the major receptor for TWEAK..
  56. pmc TWEAK binding to the Fn14 cysteine-rich domain depends on charged residues located in both the A1 and D2 modules
    Sharron A N Brown
    Department of Surgery, Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, 800 W Baltimore St, Baltimore, MD 21201, USA
    Biochem J 397:297-304. 2006
    ..These results indicate that the TWEAK-Fn14 interaction is highly dependent on multiple Fn14 residues located in both CRD modules...
  57. ncbi When are pro-inflammatory cytokines SAFE in heart failure?
    Sandrine Lecour
    Hatter Cardiovascular Research Institute, Department of Medicine, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa
    Eur Heart J 32:680-5. 2011
    ..In this review, we will discuss whether targeting the SAFE pathway may be considered as a preventive and/or therapeutic measure for the treatment of heart failure...
  58. ncbi The CD163-expressing macrophages recognize and internalize TWEAK: potential consequences in atherosclerosis
    Juan A Moreno
    Vascular Research Lab, Fundacion Jimenez Diaz, Autonoma University, Avda Reyes Catolicos 2, 28040 Madrid, Spain
    Atherosclerosis 207:103-10. 2009
    ..We have analyzed the importance of TWEAK-CD163 interaction in atherosclerosis...
  59. ncbi Induction of RANTES by TWEAK/Fn14 interaction in human keratinocytes
    Long Jin
    Atopy Allergy Research Center, Juntendo University School of Medicine, Tokyo, Japan
    J Invest Dermatol 122:1175-9. 2004
    ..Because RANTES has been implicated in inflammation, TWEAK/Fn14 interaction in human keratinocytes may be involved in the pathophysiology of inflammatory skin disorders...
  60. pmc TWEAK induces apoptosis through a death-signaling complex comprising receptor-interacting protein 1 (RIP1), Fas-associated death domain (FADD), and caspase-8
    Aminah Ikner
    Department of Molecular Oncology, Genentech, South San Francisco, California 94080, USA
    J Biol Chem 286:21546-54. 2011
    ..The proapoptotic activity of TWEAK is modulated by cIAP1 and CYLD and engages both the extrinsic and intrinsic signaling pathways...
  61. ncbi The tumor necrosis factor-like weak inducer of apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (Fn14) signaling system regulates glioma cell survival via NFkappaB pathway activation and BCL-XL/BCL-W expression
    Nhan L Tran
    Neurogenomics Division, The Translational Genomics Research Institute, Phoenix, Arizona 85004, USA
    J Biol Chem 280:3483-92. 2005
    ..Targeted therapy against Fn14 as an adjuvant to surgery may improve management of invasive glioma cells and advance the outcome of this devastating cancer...
  62. pmc TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration
    Mahasweta Girgenrath
    Boston Biomedical Research Institute, Watertown, MA, USA
    EMBO J 25:5826-39. 2006
    ....
  63. ncbi TNF-like weak inducer of apoptosis inhibits proinflammatory TNF receptor-1 signaling
    A Wicovsky
    Division of Molecular Internal Medicine, Department of Internal Medicine II, University Hospital Wurzburg, Rontgenring 11, Würzburg 97070, Germany
    Cell Death Differ 16:1445-59. 2009
    ..Taken together, we demonstrate that soluble TWEAK desensitizes cells for proinflammatory TNFR1 signaling and thus identify TWEAK as a modifier of TNF signaling...
  64. ncbi Adipocytes as immune cells: differential expression of TWEAK, BAFF, and APRIL and their receptors (Fn14, BAFF-R, TACI, and BCMA) at different stages of normal and pathological adipose tissue development
    Vassilia Ismini Alexaki
    Department of Experimental Endocrinology, University of Crete, School of Medicine, Heraklion, Greece
    J Immunol 183:5948-56. 2009
    ....
  65. pmc Membrane tumor necrosis factor (TNF) induces p100 processing via TNF receptor-2 (TNFR2)
    Hilka Rauert
    Division of Molecular Internal Medicine, Department of Internal Medicine II, University Hospital Wurzburg, Rontgenring 11, 97070 Wurzburg, Germany
    J Biol Chem 285:7394-404. 2010
    ..Thus, we identified activation of the alternative NFkappaB pathway as a TNF signaling effect that can be specifically assigned to TNFR2 and membrane TNF...
  66. pmc Soluble TWEAK and PTX3 in nondialysis CKD patients: impact on endothelial dysfunction and cardiovascular outcomes
    Mahmut Ilker Yilmaz
    Department of Nephrology, Gu lhane School of Medicine, Ankara, Turkey
    Clin J Am Soc Nephrol 6:785-92. 2011
    ..Now, we hypothesize that both sTWEAK and PTX3 act as biomarkers of cardiovascular outcomes in nondialysis CKD patients...
  67. pmc Mouse glucocorticoid-induced tumor necrosis factor receptor ligand is costimulatory for T cells
    Masahide Tone
    Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, United Kingdom
    Proc Natl Acad Sci U S A 100:15059-64. 2003
    ..Expression was controlled by the transcription factor NF-1 and potentially by alternative splicing of mRNA destabilization sequences...
  68. ncbi BAFF, APRIL, TWE-PRIL: who's who?
    Capucine Daridon
    Department of Immunopathology, Brest University Medical School, Brest, France
    Autoimmun Rev 7:267-71. 2008
    ..In order to understand the function of these molecules we need to elucidate the complexity of the various forms of these members of the TNF family...
  69. ncbi Ox-40 ligand: a potent costimulatory molecule for sustaining primary CD4 T cell responses
    I Gramaglia
    Division of Immunochemistry, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA
    J Immunol 161:6510-7. 1998
    ..These data suggest that Ox-40/Ox-40L interactions act after initial activation events to prolong clonal expansion and enhance effector cytokine secretion, and may be involved in promoting long-lived primary CD4 responses...
  70. ncbi TWEAK can induce pro-inflammatory cytokines and matrix metalloproteinase-9 in macrophages
    Se Hwa Kim
    Cardiology Division, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
    Circ J 68:396-9. 2004
    ..These results suggest that TWEAK is involved in atherosclerosis by inducing pro-inflammatory cytokines and extracellular matrix degrading enzymes, which reduce plaque stability...
  71. ncbi Epithelial NEMO links innate immunity to chronic intestinal inflammation
    Arianna Nenci
    Institute for Genetics, University of Cologne, Zulpicher Strasse 47, 50674 Cologne, Germany
    Nature 446:557-61. 2007
    ....
  72. ncbi TWEAK and Fn14: new molecular targets for cancer therapy?
    Jeffrey A Winkles
    Department of Surgery, University of Maryland Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, 21201, USA
    Cancer Lett 235:11-7. 2006
    ..In this article, we review recent studies indicating that TWEAK and Fn14 may be potential regulators of human tumorigenesis...
  73. pmc Genomic profiling of messenger RNAs and microRNAs reveals potential mechanisms of TWEAK-induced skeletal muscle wasting in mice
    Siva K Panguluri
    Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, Kentucky, United States of America
    PLoS ONE 5:e8760. 2010
    ..However, the role of miRs in skeletal muscle wasting is unknown...
  74. ncbi Tumor necrosis factor-like weak inducer of apoptosis increases the permeability of the neurovascular unit through nuclear factor-kappa B pathway activation
    Rohini Polavarapu
    Department of Neurology, Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    J Neurosci 25:10094-100. 2005
    ..We conclude that the cytokine TWEAK plays a role in the disruption of the structure and permeability of the NVU during physiological and pathological conditions...
  75. pmc In vivo kinetics of GITR and GITR ligand expression and their functional significance in regulating viral immunopathology
    Susmit Suvas
    Department of Microbiology, M409, Walters Life Sciences Building, University of Tennessee, Knoxville, TN 37996 0845, USA
    J Virol 79:11935-42. 2005
    ..Our results are the first observations to determine in vivo kinetics of GITR and GITR-L expression after virus infection, and they emphasize the role of GITR-GITR-L interaction to regulate virus-induced immuno-inflammatory lesions...
  76. ncbi Serum levels of the atherosclerosis biomarker sTWEAK are decreased in type 2 diabetes and end-stage renal disease
    Susan Kralisch
    Department of Medicine, University of Leipzig, 04103 Leipzig, Germany
    Atherosclerosis 199:440-4. 2008
    ..Furthermore, both conditions have an additive and independent negative effect on sTWEAK levels. Our results support the view that circulating sTWEAK might be a novel biomarker of atherosclerosis...
  77. ncbi TWEAK promotes ovarian cancer cell metastasis via NF-kappaB pathway activation and VEGF expression
    Lan Dai
    Department of Ob Gyn, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China
    Cancer Lett 283:159-67. 2009
    ..Targeted therapy against TWEAK-Fn14 signaling system as an adjuvant to surgery may improve clinical management of invasive ovarian cancer cells and advance the outcome of this devastating cancer...
  78. ncbi Therapeutic targeting of the effector T-cell co-stimulatory molecule OX40
    Kazuo Sugamura
    Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai 980 8575, Japan
    Nat Rev Immunol 4:420-31. 2004
  79. ncbi TWEAK and cIAP1 regulate myoblast fusion through the noncanonical NF-κB signaling pathway
    Emeka K Enwere
    Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada
    Sci Signal 5:ra75. 2012
    ..These results identify roles for TWEAK, cIAP1, and noncanonical NF-κB signaling in the regulation of myoblast fusion and highlight a role for cytokine signaling during adult skeletal myogenesis...
  80. ncbi Recycling endosome-dependent and -independent mechanisms for IL-10 secretion in LPS-activated macrophages
    A C Stanley
    Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland, Australia
    J Leukoc Biol 92:1227-39. 2012
    ..Thus, we show at least two post-Golgi pathways via which IL-10 is trafficked, ensuring its secretion from activated macrophages under different physiological conditions...
  81. ncbi TWEAK and Fn14. New players in the pathogenesis of atherosclerosis
    Luis M Blanco-Colio
    Vascular Research Lab, Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain
    Front Biosci 12:3648-55. 2007
    ..In this review, we summarize the potential proatherogenic consequences of the interaction of TWEAK with its receptor Fn14 in the vascular wall...
  82. ncbi Ox40-ligand has a critical costimulatory role in dendritic cell:T cell interactions
    A I Chen
    Immunology Research Division, Department of Pathology, Brigham and Women s Hospital and the Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Immunity 11:689-98. 1999
    ..In vitro, Ox40L-deficient dendritic cells are defective in costimulating T cell cytokine production. Thus, Ox40L has a critical costimulatory function in vitro and in vivo for dendritic cell:T cell interactions...
  83. ncbi Role of tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible 14 (Fn14) axis in rheumatic diseases
    Li Xiu Zhu
    Department of Rheumatology, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China
    Chin Med J (Engl) 125:3898-904. 2012
    ..This review discusses the role of the TWEAK-Fn14 axis in several rheumatic diseases and the potential therapeutic benefits of modulation of the TWEAK-Fn14 pathway...
  84. ncbi Tweak and FN14 in central nervous system health and disease
    Manuel Yepes
    Department of Neurology and Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    Front Biosci 12:2772-81. 2007
    ..Accordingly, here we will review the information available to this date on the role of this cytokine and its receptor in the CNS...
  85. ncbi Pro-inflammatory cytokines TNF-related weak inducer of apoptosis (TWEAK) and TNFalpha induce the mitogen-activated protein kinase (MAPK)-dependent expression of sclerostin in human osteoblasts
    Cristina Vincent
    Bone Cell Biology Group, Discipline of Orthopaedics and Trauma, University of Adelaide, and the Hanson Institute, Adelaide, Australia
    J Bone Miner Res 24:1434-49. 2009
    ..Together, our findings suggest that TWEAK, alone and with TNF, can regulate osteoblast function, at least in part by inducing sclerostin expression. Our results also suggest new roles and modes of action for sclerostin...
  86. pmc TWEAK/Fn14 interaction regulates RANTES production, BMP-2-induced differentiation, and RANKL expression in mouse osteoblastic MC3T3-E1 cells
    Takashi Ando
    Department of Immunology, Faculty of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi 409 3898, Japan
    Arthritis Res Ther 8:R146. 2006
    ..Collectively, TWEAK/Fn14 interaction regulates RANTES production, BMP-2-induced differentiation, and RANKL expression in MC3T3-E1 cells. TWEAK may thus be a novel cytokine that regulates several aspects of osteoblast function...
  87. ncbi Functional expression of TWEAK in human colonic adenocarcinoma cells
    Tomoyuki Kawakita
    First Department of Internal Medicine, Mie University School of Medicine, 2 174 Eobashi, Tsu, Mie, Japan
    Int J Oncol 26:87-93. 2005
    ..Thus, functional expression of TWEAK from human colonic adenocarcinoma cells may contribute to neovascularization...
  88. ncbi Tumor necrosis-like weak inducer of apoptosis as a proinflammatory cytokine in human adipocyte cells: up-regulation in severe obesity is mediated by inflammation but not hypoxia
    Joan Vendrell
    Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas, Hospital Universitari de Tarragona Joan XXIII, Institut d Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, 43007 Tarragona, Spain
    J Clin Endocrinol Metab 95:2983-92. 2010
    ..We previously reported the up-regulation of TNF-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible 14 (Fn14) axis in adipose tissue of severely obese type 2 diabetic subjects...
  89. ncbi Soluble TWEAK is markedly upregulated in patients with ST-elevation myocardial infarction and related to an adverse short-term outcome
    Emmanuel Chorianopoulos
    Department of Cardiology, Angiology and Pulmology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany
    Atherosclerosis 211:322-6. 2010
    ..In this retrospective pilot study we thus sought to evaluate serum levels of soluble TWEAK (sTWEAK) patients with acute ST-elevation myocardial infarction (STEMI)...
  90. ncbi OX40 is differentially expressed on activated rat and mouse T cells and is the sole receptor for the OX40 ligand
    A Al-Shamkhani
    MRC Cellular Immunology Unit, University of Oxford, GB
    Eur J Immunol 26:1695-9. 1996
    ..In addition, the new MRC OX86 mAb, unlike the MRC OX40 mAb, did not block binding of the OX40L. We conclude that OX40 is differentially expressed on activated mouse and rat T cells and is the sole receptor for the OX40L...
  91. ncbi TNF-like weak inducer of apoptosis (TWEAK) and TNF-α cooperate in the induction of keratinocyte apoptosis
    Maya Zimmermann
    Swiss Institute of Allergy and Asthma Research SIAF, University of Zurich, Davos, Switzerland
    J Allergy Clin Immunol 127:200-7, 207.e1-10. 2011
    ....
  92. pmc TWEAK and its receptor Fn14 in the synovium of patients with rheumatoid arthritis compared to psoriatic arthritis and its response to tumour necrosis factor blockade
    A W R van Kuijk
    Division of Clinical Immunology and Rheumatology, Academic Medical Center University of Amsterdam, NL 1105 AZ Amsterdam, The Netherlands
    Ann Rheum Dis 69:301-4. 2010
    ....
  93. pmc Role of TWEAK in lupus nephritis: a bench-to-bedside review
    Jennifer S Michaelson
    Immunology Discovery Biology, Biogen Idec, Cambridge, MA 02142, USA
    J Autoimmun 39:130-42. 2012
    ..Taken together, targeting the TWEAK/Fn14 axis represents a potential new therapeutic paradigm for achieving renal protection in LN patients...
  94. ncbi TWEAK/Fn14 interaction stimulates human bronchial epithelial cells to produce IL-8 and GM-CSF
    Hongri Xu
    Department of Immunology, Faculty of Medicine, University of Yamanashi, Yamanashi 409 3898, Japan
    Biochem Biophys Res Commun 318:422-7. 2004
    ..Because IL-8 and GM-CSF are associated with inflammatory conditions, these results suggest that TWEAK/Fn14 interaction may play some roles in airway inflammatory responses...
  95. pmc The interaction between tumor necrosis factor-like weak inducer of apoptosis and its receptor fibroblast growth factor-inducible 14 promotes the recruitment of neutrophils into the ischemic brain
    Woldeab B Haile
    Department of Neurology, Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    J Cereb Blood Flow Metab 30:1147-56. 2010
    ..These novel results indicate that during cerebral ischemia, the interaction between TWEAK and Fn14 leads to the recruitment of leukocytes into the ischemic tissue...
  96. ncbi FADD prevents RIP3-mediated epithelial cell necrosis and chronic intestinal inflammation
    Patrick Simon Welz
    Institute for Genetics, Centre for Molecular Medicine, University of Cologne, Zülpicher Str 47a, 50674 Cologne, Germany
    Nature 477:330-4. 2011
    ....
  97. ncbi Involvement of TWEAK/Fn14 interaction in the synovial inflammation of RA
    S Kamijo
    Department of Immunology, Juntendo University School of Medicine, 2 1 1 Hongo, Bunkyo ku, Tokyo 113 8421, Japan
    Rheumatology (Oxford) 47:442-50. 2008
    ..However, it is not clear how TWEAK takes part in the synovitis of RA. In this study, we investigated the role of TWEAK/fibroblast growth factor-inducible 14 (Fn14) interaction in the synovitis of RA...
  98. ncbi Death ligand TRAIL, secreted by CD1a+ and CD14+ cells in blister fluids, is involved in killing keratinocytes in toxic epidermal necrolysis
    Elisabeth de Araujo
    INSERM, U976, Univ Paris Diderot, Paris, F 75010, France
    Exp Dermatol 20:107-12. 2011
    ....
  99. ncbi Expression of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor-inducible 14 protein (Fn14), in healthy tissues and in tissues affected by periodontitis
    N G Kataria
    Colgate Australian Clinical Dental Research Centre, School of Dentistry, University of Adelaide, Adelaide, SA, Australia
    J Periodontal Res 45:564-73. 2010
    ..The aim of the present study was to investigate the expression of TWEAK and Fn14 at the protein and mRNA levels in gingival biopsies from periodontitis patients and from clinically healthy patients...
  100. pmc Impairment of antigen-presenting cell function in mice lacking expression of OX40 ligand
    K Murata
    Department of Microbiology and Immunology, Tohoku University School of Medicine, Sendai 980 8575, Japan
    J Exp Med 191:365-74. 2000
    ..Collectively, these results provide convincing evidence that OX40L, expressed on APCs, plays a critical role in antigen-specific T cell responses in vivo...
  101. ncbi Relationship of serum TWEAK level to cytokine level, disease activity, and response to anti-TNF treatment in patients with rheumatoid arthritis
    M C Park
    Division of Rheumatology, Department of Internal Medicine, Institute for Immunology and Immunological Diseases, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, South Korea
    Scand J Rheumatol 37:173-8. 2008
    ....

Research Grants63

  1. FUNCTIONAL ROLE OF TNF-ALPHA CYTOKINES IN BONE REPAIR
    Louis Gerstenfeld; Fiscal Year: 2004
    ..Cytokines can be grouped into three subfamilies: cysteine-knot growth factors, helical cytokines and tumor necrosis factors. The tumor necrosis factors (TNF) family of cytokines has been shown to be essential in the mediation of ..
  2. Design of Biocompatible NiTi (Nitinol) Surfaces
    PATRICIA THIEL; Fiscal Year: 2002
    ..protein adsorption, cell proliferation (peripheral blood leukocytes, THP-1 monocytes)], inflammatory mediators (expression of interlukin-1beta and tumor necrosis factors-alpha) that determine implantation outcome.
  3. VITAMIN D COMPOUNDS FOR INFLAMMATORY BOWEL DISEASE
    COLLEEN HAYES; Fiscal Year: 1999
    ..An FDA-approved short-term treatment (mouse-human IgG1 monoclonal antibody to tumor necrosis factors- alpha) has projected annual sales of $100 million...
  4. TNFR Members in T Cell Immunity to Vaccinia
    Michael Croft; Fiscal Year: 2010
    ....
  5. The Role of 4-1BB in T Cell and APC Interactions
    Michael Croft; Fiscal Year: 2010
    ..abstract_text> ..
  6. Transport of TNFalpha across the BBB
    Weihong Pan; Fiscal Year: 2008
    ..These transporters could be novel drug targets and therefore provide promising therapeutic potential. [unreadable] [unreadable]..
  7. Transport of neurotrophic cytokines after spinal cord injury
    Weihong Pan; Fiscal Year: 2007
    ..Understanding the mechanisms of cytokine transport at this regulatory interface would help in the design of new approaches to treat SCI. ..
  8. Role of TWEAK and Fn14 in Vascular Biology
    JEFFREY WINKLES; Fiscal Year: 2005
    ..It is anticipated that these studies will provide important information on the functions of the TWEAK and Fn14 proteins and their role in vascular cell biology. ..
  9. The Fn14 Receptor and Brain Tumor Invasion
    Jeffrey A Winkles; Fiscal Year: 2011
    ..The proposed studies will examine whether a protein named Fn14 contributes to tumor cell invasiveness and whether it could be a novel molecular target for anti-invasive therapy in humans. ..
  10. Vaccines to Generate Neutralizing Anti-HIV Antibodies
    RICHARD KORNBLUTH; Fiscal Year: 2008
    ..unreadable] [unreadable] [unreadable]..
  11. The Fnk Kinase and Vascular Cell Growth Control
    JEFFREY WINKLES; Fiscal Year: 2004
    ..It is anticipated that these studies will provide important information on the biological functions of the Fnk protein and its potential role in vascular cell growth control in vivo. ..
  12. Protease-Regulated Blood Brain Barrier Permeability
    Manuel Yepes; Fiscal Year: 2008
    ..unreadable] [unreadable] [unreadable]..
  13. Combined TNFSF and TLR stimulation of HIV vaccines
    RICHARD KORNBLUTH; Fiscal Year: 2006
    ..In addition, this DNA vaccine approach may prove generally applicable for emerging infections and other diseases for which a potent vaccine is needed. ..
  14. TNFSF APC activators for HIV Vaccines
    RICHARD KORNBLUTH; Fiscal Year: 2003
    ..Upon the completion of these feasibility studies, it will be clear if these concepts should be advanced into more extensive vaccine studies both for HIV and other pathogens. ..
  15. Regulation of HIV-1 Preintegration Complexes (PICs)
    RICHARD KORNBLUTH; Fiscal Year: 2002
    ..New tools and concepts will be gained, and precise molecular targets for anti-HIV drug design will come into focus. ..
  16. Nuclear Function of the c-Abl Protooncoprotien
    Jean Wang; Fiscal Year: 2007
    ..Aim 6 will implement two strategies to identify other nuclear substrates of c-Abl. Identification of substrates will provide further information on the biological function of the c-Abl tyrosine kinase. ..
  17. DECIDUAL CELL/PLACENTAL INTERACTIONS
    JOAN HUNT; Fiscal Year: 2007
    ..abstract_text> ..
  18. Mitogen-activated Protein Kinases and NF-kB Activation in Vascular Smooth Muscle
    Bingbing Jiang; Fiscal Year: 2010
    ....
  19. Mechanisms of T-cell induced-APC cytotoxicity in lupus
    Mariana Kaplan; Fiscal Year: 2006
    ..The sponsor and the institution are committed to contributing protected time, career development and resources to the applicant. ..
  20. Impaired Tumoricidal Activity Of DCs in HNC Patients
    Nikola Vujanovic; Fiscal Year: 2006
    ..The proposed study will define biological and clinical relevance of DC tumoricidal activity and is likely to lead to development of more potent DC-based vaccines for prevention and therapy of HNC. ..
  21. The role of dendritic cell-T cell interactions in the p*
    Mariana Kaplan; Fiscal Year: 2006
    ..These could lead into the development of novel therapeutic interventions designed to reverse these abnormalities and abrogate or block the onset and/or severity of this disease. ..
  22. FUNCTION OF NOGGIN IN HAIR FOLLICLE GROWTH AND DISEASE
    Vladimir Botchkarev; Fiscal Year: 2006
    ....
  23. Inflammation Pathways in Breast Cancer
    Margaret M Madeleine; Fiscal Year: 2010
    ..Cytokine genes are expressed at different levels in older compared to younger women;therefore, we will also evaluate their contribution to breast cancer risk by levels of common exposures such as obesity and HRT use. ..
  24. A Canine Model for Human X-Linked Ectodermal Dysplasia
    Margret Casal; Fiscal Year: 2007
    ..Furthermore, the HED dogs will be examined to demonstrate that a specific immune deficiency is responsible for pulmonary disease rather than the previously thought lack of respiratory mucoid glands. ..
  25. Alcohol-specific modifications of glycated Hb: Novel biomarkers of alcohol abuse
    Yousef Al Abed; Fiscal Year: 2007
    ..Future studies will be designed to measure these alcohol-specific-markers in humans following binge and chronic alcohol intake. [unreadable] [unreadable] [unreadable]..
  26. Protein Tyrosine Kinases in Leiomyomata Uteri
    Jean Wang; Fiscal Year: 2007
    ..Information gathered from the proposed research may therefore lead to the development of new therapeutics to control the growth of fibroids. ..
  27. Chemokin Regulation of Cartilage Matrix Resorption
    Lei Wei; Fiscal Year: 2008
    ..abstract_text> ..
  28. TNF Signaling in Neurodegeneration
    MARIALOURDES G TANSEY; Fiscal Year: 2010
    ....
  29. Regulatory T cells in transplantation tolerance
    James Markmann; Fiscal Year: 2008
    ..Collectively, these studies will further our understanding of regulatory T cell function in vivo and help to define their potential for application in the clinical transplant arena. ..
  30. Lymphocyte recruitment in alcoholic hepatitis
    David Adams; Fiscal Year: 2009
    ..abstract_text> ..
  31. T Cell Memory to Respiratory Viral Infections
    Shahram Salek Ardakani; Fiscal Year: 2008
    ..unreadable] [unreadable] [unreadable] [unreadable]..
  32. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 2007
    ..abstract_text> ..
  33. Chemokine and antigen-carrying nanoparticle co-delivery for an oral HIV vaccine
    DARRELL IRVINE; Fiscal Year: 2008
    ..unreadable] [unreadable] [unreadable]..
  34. Imaging Cytokine Transfer at the Immunological Synapse
    DARRELL IRVINE; Fiscal Year: 2006
    ..abstract_text> ..
  35. ROLE OF THE FAS ANTIGEN IN OVARIAN CELL APOPTOSIS
    SUSAN QUIRK; Fiscal Year: 2004
    ..Understanding pathways that promote or prevent susceptibility of ovarian cells to apoptosis may lead to development of novel therapies for ovarian and other cancers. ..
  36. Immunoregulation in Cyclosporine-Induced Autoimmunity
    Allan Hess; Fiscal Year: 2003
    ..This unique model and the proposed studies will provide novel insights into systemic control of autoaggression. ..
  37. Induction of Apoptosis in Synovial Fibroblasts
    Haidi Zhang; Fiscal Year: 2003
    ..at an early stage of arthritis by intra-articular administration of an apoptosis inducer, such as FasL, using a suitable vector system, which may replace the treatment of synovectomy for some arthritis patients. ..
  38. DEPRESSION AND TRIAL OF VARICELLA VACCINE IN THE ELDERLY
    Michael Irwin; Fiscal Year: 2003
    ....
  39. INVARIANT CHAIN BASED VACCINE STRATEGIES
    Allan Hess; Fiscal Year: 2003
    ..These studies will identify novel strategies to enhance the immunogenicity of tumor peptides that may be broadly applicable to many different types of cancer. ..
  40. A ROLE FOR NOGGIN AND BMP2/4 IN HAIR GROWTH CONTROL
    Vladimir Botchkarev; Fiscal Year: 2003
    ..abstract_text> ..
  41. Chlamydia trachomatis and Cervical Cancer
    MARGARET MADELEINE; Fiscal Year: 2003
    ..trachomatis may become a higher public health priority. Furthermore, our results would help determine whether further follow up of the C. trachomatis and cervical cancer association is warranted in a more expensive, prospective setting. ..
  42. BEHAVIORAL INTERVENTION FOR HERPES ZOSTER RISK IN AGING
    Michael Irwin; Fiscal Year: 2003
    ....
  43. REGULATION OF HELPER T CELL MEMORY
    Linda Bradley; Fiscal Year: 2002
    ..The proposed studies represents an integrated investigation of factors that will provide essential, basic information about the regulation of CD4 memory. ..
  44. MECHANISMS OF STRESS-INDUCED APOPTOSIS IN T CELLS
    Douglas Green; Fiscal Year: 2001
    ..His focus on T lymphocytes is important in the context of understanding how the immune system responds to DNA damage and related stress to remove potentially damaged cells, that could otherwise pose a threat to immune integrity. ..
  45. INDUCTION AND ANALYSIS OF PROSTATE CANCER
    James Norris; Fiscal Year: 2001
    ....
  46. THE FUNCTION OF T-BET IN T HELPER CELL DEVELOPMENT
    Stanford Peng; Fiscal Year: 2003
    ..abstract_text> ..
  47. TRANSDUCTION OF CHRONIC NERVE INJURY BY SCHWANN CELLS
    Ranjan Gupta; Fiscal Year: 2004
    ..Successful completion of these studies will provide a greater understanding of the pathogenesis of CNI so that more effective treatment modalities may be developed. ..
  48. Tumor-reactive IgG in the diagnosis of ovarian cancer
    Douglas Taylor; Fiscal Year: 2005
    ..Ultimately, antigenic proteins, linked with histologic type and stage of disease, will be combined into the development of protein arrays to screen for circulating reactive IgG as an early diagnostic test. ..
  49. Epo-dependent JAK2 Signaling in Painful Neuropathy
    WENDY CAMPANA; Fiscal Year: 2006
    ..The experiments will provide new information on the basic mechanisms of nerve injury and pain, and there from, new rationale for development of novel neuroprotective strategies for preventing chronic neuropathic pain. ..
  50. RESEARCH PERSPECTIVES IN PNI, TRAINEE TRAVEL
    Michael Irwin; Fiscal Year: 2006
    ..abstract_text> ..
  51. Proteomics of altered protein in macular degeneration
    DEBORAH FERRINGTON; Fiscal Year: 2006
    ..Identification of proteins that are uniquely altered will help provide valuable insight into the mechanism of AMD. ..
  52. Mouse model of oral infection with virulent Francisella
    Wangxue Chen; Fiscal Year: 2005
    ..tularensis infection so that future hypothesis-driven studies with more focused research objectives can be designed and developed. ..
  53. Vaccine-driven modulation of dendritic cell trafficking
    DARRELL IRVINE; Fiscal Year: 2005
    ..abstract_text> ..
  54. Microsimulation of anthracis-immune system interaction
    THOMAS KEPLER; Fiscal Year: 2005
    ....
  55. Cocaine Dependence: EEG Sleep and Cytokines
    Michael Irwin; Fiscal Year: 2005
    ..abstract_text> ..
  56. MOLECULAR MECHANISMS OF CHEMOTHERAPY-INDUCED HAIR LOSS
    Vladimir Botchkarev; Fiscal Year: 2005
    ..Patients with many forms of p53-negative cancers treated by chemotherapy may ultimately benefit from this study. ..
  57. Conference on Cellular Senescene and Cell Death
    Douglas Green; Fiscal Year: 2005
    ..The interconnections between these biological events and the overlapping principles that emerge represent an emerging field in biology and biomedical research. ..
  58. Tai Chi Effects on Chronic Insomnia in Breast Cancer Survivors: Immune Mechanisms
    Michael R Irwin; Fiscal Year: 2010
    ..This project will constitute the first, randomized controlled clinical trial of the effects of TCC on sleep outcomes in breast cancer survivors, and will advance psychobiological models of insomnia treatment mechanisms. ..
  59. Alcoholism: Sleep and Cytokines in African Americans
    Michael Irwin; Fiscal Year: 2005
    ..g., cytokine antagonists) for sleep disturbance in alcoholism. ..
  60. Sleep and Immune Mechanisms in Rheumatoid Arthritis
    Michael Irwin; Fiscal Year: 2009
    ..Results from this study will guide the development of interventions that target disordered sleep with potential effects on disability in RA. ..
  61. Modulating Lymphotoxins for Viral Defenses
    Carl Ware; Fiscal Year: 2009
    ..The success of these reagents should validate this novel immunotherapeutic approach as a potential treatment for human CMV infection. ..
  62. CHEMOKINE BIOLOGY IN BRONCHIOLITIS OBLITERANS SYNDROME
    John Belperio; Fiscal Year: 2005
    ..The understanding of this pathobiology will lead to novel therapies in the treatment and prevention of chronic lung allograft rejection, BOS. ..