Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 41, Issue 11, Pages 3351-3360Publisher
WILEY
DOI: 10.1002/eji.201141629
Keywords
CD8(+) T cells; Cellular activation; Cytokines; Signal transduction
Categories
Funding
- NIH [AI063496, K99/R00HL97155]
- NSFC [30528008, 30700728]
- Cancer Research Institute
- Eleven-Fifth Mega-Scientific Project on 'Prevention and treatment of AIDS, viral hepatitis and other infectious diseases' [2008ZX10003-012]
- China Scholarship council [2010692006]
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The effector functions of CD8(+) T cells are influenced by tissue inflammatory micro-environments. IL-33, a member of the IL-1 family, acts as a danger signal after its release during cell necrosis. The IL-33/ST2 axis has been implicated in various Th2 responses. Its role in CD8(+) T-cell-mediated immune response is, however, not known. Here we find that type 1 cytotoxic T (Tc1) cells cultured in vitro unexpectedly express high levels of the IL-33 receptor ST2. Interestingly, the expression of ST2 in Tc1 cells is dependent on T-bet, a master Th1/Tc1 transcription factor. In addition, IL-33 enhances TCR-triggered IFN-gamma production. IL-33 together with IL-12 can stimulate IFN-gamma production in Tc1 cells. Moreover, IL-33 synergizes with IL-12 to promote CD8(+) T-cell effector function. The synergistic effect of IL-33 and IL-12 is partly mediated by Gadd45b. Together, these in vitro data establish a novel role of IL-33 in promoting effector type 1 adaptive immune responses.
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