Interferon-β mediates stromal cell rescue of T cells from apoptosis
Research output: Contribution to journal › Article › peer-review
Authors
Colleges, School and Institutes
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 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 T cell survival in a resting G(0)/G(1) state. We now report that interferon-beta is the principal mediator of stromal cell-mediated T cell rescue from apoptosis. Interferon-alpha and -beta 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.
Details
Original language | English |
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Pages (from-to) | 1041-1050 |
Number of pages | 10 |
Journal | European Journal of Immunology |
Volume | 29 |
Issue number | 3 |
Publication status | Published - 1 Mar 1999 |