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Immunological tolerance to a pancreatic antigen as a result of local expression of TNFalpha by islet beta cells.

Abstract：

:Recent experiments have suggested that tumor necrosis factor alpha (TNFalpha) can down-regulate islet-specific T cells and prevent the development of autoimmune diabetes. Here we demonstrate that transgenic mice expressing both TNFalpha and the Leishmania major LACK antigen in the pancreas (RIP-TNFalpha/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-TNFalpha/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 TNFalpha may act in vivo to modulate a potentially damaging self-reactive T cell response by inducing tolerance to pancreatic antigens.

journal_name

Immunity

journal_title

Immunity

authors

McSorley SJ,Soldera S,Malherbe L,Carnaud C,Locksley RM,Flavell RA,Glaichenhaus N

doi

10.1016/s1074-7613(00)80361-1

subject

Has Abstract

pub_date

1997-09-01 00:00:00

pages

401-9

issue

3

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(00)80361-1

journal_volume

7

pub_type

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