Abstract
Insulin-dependent diabetes mellitus results from T-cell-mediated destruction of pancreatic islet β cells. Both CD4 and CD8 T cells have been shown to be independently capable of β cell destruction. However, the mechanism of β cell destruction has remained elusive. It has previously been shown that the absence of TNF-α receptor I (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-α receptor I (p55) deficient islets induce similar levels of proliferation of BDC2.5 T cells. In this study, we demonstrate that islet TNF-α 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.
Original language | English (US) |
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Pages (from-to) | 198-207 |
Number of pages | 10 |
Journal | Clinical Immunology |
Volume | 100 |
Issue number | 2 |
DOIs | |
State | Published - 2001 |
Externally published | Yes |
Keywords
- Autoimmunity
- Diabetes
- HVEM
- LIGHT
- T cells
- TNF-α receptor
ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
- Pathology and Forensic Medicine