Journal
CLINICAL IMMUNOLOGY
Volume 100, Issue 2, Pages 198-207Publisher
ACADEMIC PRESS INC
DOI: 10.1006/clim.2001.5059
Keywords
autoimmunity; diabetes; TNF-alpha receptor; T cells; LIGHT; HVEM
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Funding
- NIDDK NIH HHS [DK 57644-01] Funding Source: Medline
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Insulin-dependent diabetes mellitus results from T-cell-mediated destruction of pancreatic islet beta cells. Both CD4 and CD8 T cells have been shown to be independently capable of beta cell destruction. However, the mechanism of beta cell destruction has remained elusive. It has previously been shown that the absence of TNF-alpha receptor 1 (p55) on the islets protected islets from CD4 T-cell-mediated destruction as long as the T cells did not have access to wild-type islets in vivo. Wild-type and TNF-alpha receptor 1 (p55) deficient islets induce similar levels of proliferation of BDC2.5 T cells. In this study, we demonstrate that islet TNF-alpha receptor I (p55) influences the expression of LIGHT (TNFSF-14), a TNF family member with both cytolytic and costimulatory properties, on BDC2.5 T cells and the expression of its receptor HVEM (TNFRSF-14) by islets, indicating a role for LIGHT-HVEM interactions in autoimmune diabetes. (C) 2001 Academic Press.
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