Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 191, Issue 7, Pages 1095-1103Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.191.7.1095
Keywords
autoimmunity; inflammation; apoptosis; cytokine; TRAIL
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Funding
- NIAID NIH HHS [AI41060] Funding Source: Medline
- NIAMS NIH HHS [AR44914] Funding Source: Medline
- NINDS NIH HHS [NS53681] Funding Source: Medline
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The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis of tumor cells but not normal cells; its role in normal nontransformed tissues is unknown. We report here that chronic blockade of TRAIL in mice exacerbated autoimmune arthritis, and that intraarticular TRAIL gene transfer ameliorated the disease. In vivo, TRAIL blockade led to profound hyperproliferation of synovial cells and arthritogenic lymphocytes and heightened the production of cytokines and autoantibodies. In vitro, TRAIL inhibited DNA synthesis and prevented cell cycle progression of lymphocytes. Interestingly, TRAIL had Ilo effect on apoptosis of inflammatory cells either in vivo or in vitro. Thus, unlike other members of the tumor necrosis factor superfamily, TRAIL is a prototype inhibitor protein that inhibits autoimmune inflammation by blocking cell cycle progression.
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