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Immunity. 2013 Oct 17;39(4):661-75. doi: 10.1016/j.immuni.2013.08.032. Epub 2013 Oct 10.

Epigenetic modifications induced by Blimp-1 Regulate CD8⁺ T cell memory progression during acute virus infection.

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Dept. of Pathology, University of Massachusetts Medical School, Worcester, MA 01655, USA.
Dept. of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA and Howard Hughes Medical Institute.
Contributed equally


The transcription factor Blimp-1 regulates the overall accumulation of virus-specific CD8⁺ T cells during acute viral infections. We found that increased proliferation and survival of Blimp-1-deficient CD8⁺ T cells resulted from sustained expression of CD25 and CD27 and persistent cytokine responsiveness. Silencing of Il2ra and Cd27 reduced the Blimp-1-deficient CD8⁺ T cell response. Genome-wide chromatin immunoprecipitation (ChIP) sequencing analysis identified Il2ra and Cd27 as direct targets of Blimp-1. At the peak of the antiviral response, but not earlier, Blimp-1 recruited the histone-modifying enzymes G9a and HDAC2 to the Il2ra and Cd27 loci, thereby repressing expression of these genes. In the absence of Blimp-1, Il2ra and Cd27 exhibited enhanced histone H3 acetylation and reduced histone H3K9 trimethylation. These data elucidate a central mechanism by which Blimp-1 acts as an epigenetic regulator and enhances the numbers of short-lived effector cells while suppressing the development of memory-precursor CD8⁺ T cells.

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