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Publication : PRDM16 regulates γδT17 cell differentiation via controlling type 17 program and lipid-dependent cell fitness.

First Author  Nah J Year  2023
Journal  Front Immunol Volume  14
Pages  1332386 PubMed ID  38239368
Mgi Jnum  J:348757 Mgi Id  MGI:7575055
Doi  10.3389/fimmu.2023.1332386 Citation  Nah J, et al. (2023) PRDM16 regulates gammadeltaT17 cell differentiation via controlling type 17 program and lipid-dependent cell fitness. Front Immunol 14:1332386
abstractText  gammadeltaT17 cells are a subset of gammadeltaT cells producing IL-17, which is crucial for protection against bacterial and fungal infections. It has recently been shown that gammadeltaT17 cells have enriched lipid storage and lipid metabolism. However, the regulation of gammadeltaT17 cell function and differentiation with respect to lipids remains unknown. Here, we report that PRDM16 is a critical regulator of gammadeltaT17 cell differentiation, controlling type 17 immunity gene expression program and lipid-dependent cell fitness. We demonstrated that gammadeltaT17 cells have higher lipid-dependent cell fitness, which is negatively correlated with the expression of Prdm16. Loss of Prdm16 enhances the function and differentiation of gammadeltaT17 cells, and increases their fitness in lipid-rich environments. Specifically, loss of Prdm16 exacerbates development of psoriasis in the skin, a lipid-rich organ, and Prdm16 controls lipid-mediated differentiation of Vgamma4(+) gammadeltaT17 cells, which are the major source of IL-17 during the onset of psoriasis. Our study highlights the potential impact of PRDM16 on lipid-dependent fitness and protective immune function of gammadeltaT cells and also on the immunotherapy of psoriasis and inflammatory diseases.
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