TNF-α receptor 1 (p55) on islets is necessary for the expression of LIGHT on diabetogenic T cells

Syamasundar V. Pakala, Alex Ilic, Lie Ping Chen, Nora Sarvetnick

Research output: Contribution to journalArticle

8 Scopus citations

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 languageEnglish (US)
Pages (from-to)198-207
Number of pages10
JournalClinical Immunology
Volume100
Issue number2
DOIs
StatePublished - 2001

Keywords

  • Autoimmunity
  • Diabetes
  • HVEM
  • LIGHT
  • T cells
  • TNF-α receptor

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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