IL-17-committed Vg4+ gd T cell deficiency in a spontaneous Sox13 mutant CD45.1 congenic mouse substrain protects from dermatitis
IL-17-committed ?d T (?dT17) cells participate in many immune responses but their developmental requirements and subset specific functions remain poorly understood. Here we report that a commonly used CD45.1+ congenic C57BL/6 mouse substrain is characterized by a selective deficiency in V?4+ ?dT17 cells. This trait is due to a spontaneous mutation in the transcription factor Sox13 that causes an intrinsic defect in development of these cells in the neonatal thymus. ?dT17 cells migrate at low rates from skin to lymph nodes. In a model of psoriasis-like dermatitis, V?4+ ?dT17 cells expand markedly in lymph nodes and home to inflamed skin. Sox13 mutant mice are protected from psoriasis-like skin changes, identifying a role for Sox13-dependent ?dT17 cells in this inflammatory condition.