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Immunity. 2016 Jan 19;44(1):131-142. doi: 10.1016/j.immuni.2015.11.009. Epub 2015 Dec 29.

Interleukin-23-Induced Transcription Factor Blimp-1 Promotes Pathogenicity of T Helper 17 Cells.

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Merck Research Laboratories, 901 California Avenue, Palo Alto, CA 94304, USA.
Molecular Immunology and Inflammation Branch, National Institute of Arthritis, & Musculoskeletal and Skin Diseases, National Institute of Health, Bethesda, MD 20892, USA.
Merck Research Laboratories, 901 California Avenue, Palo Alto, CA 94304, USA. Electronic address:


Interleukin-23 (IL-23) is a pro-inflammatory cytokine required for the pathogenicity of T helper 17 (Th17) cells but the molecular mechanisms governing this process remain unclear. We identified the transcription factor Blimp-1 (Prdm1) as a key IL-23-induced factor that drove the inflammatory function of Th17 cells. In contrast to thymic deletion of Blimp-1, which causes T cell development defects and spontaneous autoimmunity, peripheral deletion of this transcription factor resulted in reduced Th17 activation and reduced severity of autoimmune encephalomyelitis. Furthermore, genome-wide occupancy and overexpression studies in Th17 cells revealed that Blimp-1 co-localized with transcription factors RORγt, STAT-3, and p300 at the Il23r, Il17a/f, and Csf2 cytokine loci to enhance their expression. Blimp-1 also directly bound to and repressed cytokine loci Il2 and Bcl6. Taken together, our results demonstrate that Blimp-1 is an essential transcription factor downstream of IL-23 that acts in concert with RORγt to activate the Th17 inflammatory program.

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