Deficiency in IL-17-committed Vγ4+ γδ T cells in a spontaneous Sox13-mutant CD45.1+ congenic mouse substrain provides protection from dermatitis

Interleukin 17 (IL-17)-committed gamma delta T cells (gamma delta T17 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 selective deficiency in V(gamma)4(+) gamma delta T17 cells. This trait was due to a spontaneous mutation in the gene encoding the transcription factor Sox13 that caused an intrinsic defect in development of those cells in the neonatal thymus. The gdT17 cells migrated from skin to lymph nodes at low rates. In a model of psoriasis-like dermatitis, the V(gamma)4(+) gamma delta T17 cell subset expanded considerably in lymph nodes and homed to inflamed skin. Sox13-mutant mice were protected from psoriasis-like skin changes, which identified a role for Sox13-dependent gamma delta T17 cells in this inflammatory condition.