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

Syamasundar V. Pakala, Alex Ilic, LiePing Chen, Nora Sarvetnick

Research output: Contribution to journalArticle

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
Externally publishedYes

Fingerprint

T-Lymphocytes
Light
Type 1 Diabetes Mellitus
Islets of Langerhans
recombinant human tumor necrosis factor-binding protein-1

Keywords

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

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Pathology and Forensic Medicine

Cite this

TNF-α receptor 1 (p55) on islets is necessary for the expression of LIGHT on diabetogenic T cells. / Pakala, Syamasundar V.; Ilic, Alex; Chen, LiePing; Sarvetnick, Nora.

In: Clinical Immunology, Vol. 100, No. 2, 2001, p. 198-207.

Research output: Contribution to journalArticle

Pakala, Syamasundar V. ; Ilic, Alex ; Chen, LiePing ; Sarvetnick, Nora. / TNF-α receptor 1 (p55) on islets is necessary for the expression of LIGHT on diabetogenic T cells. In: Clinical Immunology. 2001 ; Vol. 100, No. 2. pp. 198-207.
@article{173fce1afd764691b54f9e94242526be,
title = "TNF-α receptor 1 (p55) on islets is necessary for the expression of LIGHT on diabetogenic T cells",
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.",
keywords = "Autoimmunity, Diabetes, HVEM, LIGHT, T cells, TNF-α receptor",
author = "Pakala, {Syamasundar V.} and Alex Ilic and LiePing Chen and Nora Sarvetnick",
year = "2001",
doi = "10.1006/clim.2001.5059",
language = "English (US)",
volume = "100",
pages = "198--207",
journal = "Clinical Immunology",
issn = "1521-6616",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - TNF-α receptor 1 (p55) on islets is necessary for the expression of LIGHT on diabetogenic T cells

AU - Pakala, Syamasundar V.

AU - Ilic, Alex

AU - Chen, LiePing

AU - Sarvetnick, Nora

PY - 2001

Y1 - 2001

N2 - 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.

AB - 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.

KW - Autoimmunity

KW - Diabetes

KW - HVEM

KW - LIGHT

KW - T cells

KW - TNF-α receptor

UR - http://www.scopus.com/inward/record.url?scp=0034905174&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034905174&partnerID=8YFLogxK

U2 - 10.1006/clim.2001.5059

DO - 10.1006/clim.2001.5059

M3 - Article

C2 - 11465949

AN - SCOPUS:0034905174

VL - 100

SP - 198

EP - 207

JO - Clinical Immunology

JF - Clinical Immunology

SN - 1521-6616

IS - 2

ER -