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Significance Invariant natural killer T (iNKT) cells are innate-like T cells that recognize lipid antigens and play important roles in antimicrobial and tumor immunity. Functionally, iNKT cells have been classified in three effector subsets based on expression of specific transcription factors (TFs) and cytokine genes. We previously demonstrated that the TF Bcl11b controls glycolipid processing and presentation by double-positive thymocytes to iNKT precursors and thus their formation. Using a model that allows bypassing those defects, here we provide evidence that the TF Bcl11b is critical for effector iNKT1 and INKT2 subsets and overall survival of iNKT cells. Additionally we provide evidence that Bcl11b sustains cytokine production by iNKT1 and iNKT2 cells and restricts expression of the iNKT17 cell program in all effector subsets.

Transcription factor Bcl11b sustains iNKT1 and iNKT2 cell programs, restricts iNKT17 cell program, and governs iNKT cell survival