Cutting-edge: Bcl-3 up-regulation by signal 3 cytokine (IL-12) prolongs survival of antigen-activated CD8 T cells

Javier O. Valenzuela, Christopher D. Hammerbeck, Matthew F. Mescher

Research output: Contribution to journalArticle

72 Scopus citations

Abstract

Clonal expansion of T cells requires cell division and survival during the proliferative phase of the response. Naive murine CD8 T cells responding to Ag and costimulation undergo an abortive response characterized by impaired clonal expansion, failure to develop effector functions, and long-term tolerance. A third signal provided by IL-12 is required for full expansion, activation, and establishment of memory. The enhanced survival, and thus clonal expansion, supported by IL-12 is not due to increased Bcl-2 or Bcl-xL expression; both are maximally activated by signals 1 and 2. In contrast, Bcl-3, recently shown to enhance survival when ectopically expressed in T cells, is increased only when IL-12 is present. Furthermore, examination of Bcl-3-deficient CD8 T cells demonstrates that the increased survival caused by IL-12 depends upon Bcl-3. The time courses of expression suggest that Bcl-2 and Bcl-xL promote survival early in the response, whereas Bcl-3 acts later in the response.

Original languageEnglish (US)
Pages (from-to)600-604
Number of pages5
JournalJournal of Immunology
Volume174
Issue number2
DOIs
StatePublished - Jan 15 2005

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