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Interferon‐β mediates stromal cell rescue of T cells from apoptosis
Author(s) -
Pilling Darrell,
Akbar Arne N.,
Girdlestone John,
Orteu Catherine H.,
Borthwick Nicola J.,
Amft Nicole,
ScheelToellner Dagmar,
Buckley Christopher D.,
Salmon Mike
Publication year - 1999
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/(sici)1521-4141(199903)29:03<1041::aid-immu1041>3.0.co;2-#
Subject(s) - stromal cell , biology , microbiology and biotechnology , inflammation , immune system , mediator , t cell , apoptosis , immunology , interferon , cancer research , biochemistry
Abstract The resolution of immune responses is characterized by extensive apoptosis of activated T cells. However, to generate and maintain immunological memory, some antigen‐specific T cells must survive and revert to a resting G 0 /G 1 state. Cytokines that bind to the common γ chain of the IL‐2 receptor promote the survival of T cell blasts, but also induce proliferation. In contrast, soluble factors secreted by stromal cells induce T cell survival in a resting G 0 /G 1 state. We now report that interferon‐β is the principal mediator of stromal cell‐mediated T cell rescue from apoptosis. Interferon‐α and ‐β promote the reversion of blast T cells to a resting G 0 /G 1 configuration with all the characteristic features of stromal cell rescue; such as high Bcl‐X L expression and low Bcl‐2. Type I interferons and stromal cells stimulate apparently identical signaling pathways, leading to STAT‐1 activation. We also show that this mechanism may play a fundamental role in the persistence of T cells at sites of chronic inflammation; suggesting that chronic inflammation is an aberrant consequence of immunological memory.