Nature Immunology
- 7, 1317 - 1325 (2006)
Published online: 5 November 2006; | doi:10.1038/ni1403
Transcriptional regulator Id2 mediates CD8+ T cell immunityMichael A Cannarile1, 3, Nicholas A Lind1, 3, Richard Rivera2, Alison D Sheridan1, Kristin A Camfield1, Bei Bei Wu1, Kitty P Cheung1, Zhaoqing Ding1 & Ananda W Goldrath11
Division of Biological Sciences, University of California, San Diego, La Jolla, California 92093, USA. 2
Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037, USA. 3
These authors contributed equally to this work.
Correspondence should be addressed to Ananda W Goldrath agoldrath@ucsd.edu Transcriptional programs that initiate and sustain the proliferation, differentiation and survival of CD8+ T cells during immune responses are not completely understood. Here we show that inhibitor of DNA binding 2 (Id2), an antagonist of E protein transcription factors, was upregulated in CD8+ T cells during infection and that expression of Id2 was maintained in memory CD8+ T cells. Although Id2-deficient naive CD8+ T cells recognized antigen and proliferated normally early after infection, effector CD8+ T cells did not accumulate because the cells were highly susceptible to apoptosis. Id2-deficient CD8+ T cells responding to infection had changes in the expression of genes that influence survival and had altered memory formation. Our data emphasize the importance of Id2 in regulating gene expression by CD8+ T cells and the magnitude of effector responses, suggesting a mechanism involving Id protein– and E protein–mediated survival and differentiation of mature T cells.
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