PubMed:10092109 JSONTXT

{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":71},"obj":"Sentence"},{"id":"T2","span":{"begin":72,"end":168},"obj":"Sentence"},{"id":"T3","span":{"begin":169,"end":304},"obj":"Sentence"},{"id":"T4","span":{"begin":305,"end":441},"obj":"Sentence"},{"id":"T5","span":{"begin":442,"end":544},"obj":"Sentence"},{"id":"T6","span":{"begin":545,"end":659},"obj":"Sentence"},{"id":"T7","span":{"begin":660,"end":864},"obj":"Sentence"},{"id":"T8","span":{"begin":865,"end":982},"obj":"Sentence"},{"id":"T9","span":{"begin":983,"end":1196},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":71},"obj":"Sentence"},{"id":"T2","span":{"begin":72,"end":168},"obj":"Sentence"},{"id":"T3","span":{"begin":169,"end":304},"obj":"Sentence"},{"id":"T4","span":{"begin":305,"end":441},"obj":"Sentence"},{"id":"T5","span":{"begin":442,"end":544},"obj":"Sentence"},{"id":"T6","span":{"begin":545,"end":659},"obj":"Sentence"},{"id":"T7","span":{"begin":660,"end":864},"obj":"Sentence"},{"id":"T8","span":{"begin":865,"end":982},"obj":"Sentence"},{"id":"T9","span":{"begin":983,"end":1196},"obj":"Sentence"}],"text":"Interferon-beta mediates stromal cell rescue of T cells from apoptosis.\nThe 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."}

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