Immunological tolerance to a pancreatic antigen as a result of local expression of TNFα by islet β cells

Stephen J Mcsorley, Sylvelie Soldera, Laurent Malherbe, Claude Carnaud, Richard M. Locksley, Richard A. Flaveil, Nicolas Glaichenhaus

Research output: Contribution to journalArticle

43 Scopus citations

Abstract

Recent experiments have suggested that tumor necrosis factor α (TNFα) can down-regulate islet-specific T cells and prevent the development of autoimmune diabetes. Here we demonstrate that transgenic mice expressing both TNFα and the Leishmania major LACK antigen in the pancreas (RIP-TNFα/RIP- LACK) exhibit an impaired ability to mount a CD4+ T cell response against LACK. In addition, peripheral CD4+ T cells from TCR transgenic mice (TCR- LACK/RIP-TNFα/RIP-LACK) produced reduced interleukin-2 but elevated levels of T helper 2 cytokines in response to LACK peptide in vitro. Taken together, our data suggest that TNFα may act in vivo to modulate a potentially damaging self-reactive T cell response by inducing tolerance to pancreatic antigens.

Original languageEnglish (US)
Pages (from-to)401-409
Number of pages9
JournalImmunity
Volume7
Issue number3
DOIs
StatePublished - Sep 1997
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases
  • Immunology

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    Mcsorley, S. J., Soldera, S., Malherbe, L., Carnaud, C., Locksley, R. M., Flaveil, R. A., & Glaichenhaus, N. (1997). Immunological tolerance to a pancreatic antigen as a result of local expression of TNFα by islet β cells. Immunity, 7(3), 401-409. https://doi.org/10.1016/S1074-7613(00)80361-1