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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 G0/G1 state. Cytokines that bind to the common gamma 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 Tcell survival in a resting G0/G1 state. We now report that interferon-beta is the principal mediator of stromal cell-mediated Tcell rescue from apoptosis. Interferon-alpha and -beta promote the reversion of blast Tcells to a resting G0/G1 configuration with all the characteristic features of stromal cell rescue; such as high Bcl-XL 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.

Original publication

DOI

10.1002/(SICI)1521-4141(199903)29:03<1041::AID-IMMU1041>3.0.CO;2-#

Type

Journal article

Journal

Eur J Immunol

Publication Date

03/1999

Volume

29

Pages

1041 - 1050

Keywords

Apoptosis, Arthritis, Rheumatoid, DNA-Binding Proteins, Fibroblasts, Humans, Immunophenotyping, Interferon-alpha, Interferon-beta, Milk Proteins, STAT1 Transcription Factor, STAT5 Transcription Factor, Signal Transduction, Stromal Cells, Synovial Fluid, T-Lymphocytes, Trans-Activators