Deficiency in IL-17-committed Vγ4(+) γδ T cells in a spontaneous Sox13-mutant CD45.1(+) congenic mouse substrain provides protection from dermatitis.
Deficiency in IL-17-committed Vγ4(+) γδ T cells in a spontaneous Sox13-mutant CD45.1(+) congenic mouse substrain provides protection from dermatitis.
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il -17介导的γδT （γδ t17）细胞参与许多免疫应答，但其发育要求和亚群特异性功能尚不清楚。在这里，我们报告了一种常用的CD45.1+同源C57BL/6小鼠亚株的特征是Vγ4+ γδT17细胞的选择性缺陷。这种特性是由于转录因子Sox13的自发突变导致新生儿胸腺这些细胞发育的内在缺陷。γδT17细胞从皮肤向淋巴结的迁移速率较低。在银屑病样皮炎模型中，v - γ4+ γδT17细胞在淋巴结中显著扩增，并返回炎症皮肤。Sox13突变小鼠免受牛皮癣样皮肤变化的影响，确定了Sox13依赖性γδT17细胞在这种炎症状况中的作用。
IL-17-committed γδ T (γδT17) 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 Vγ4+ γδT17 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. γδT17 cells migrate at low rates from skin to lymph nodes. In a model of psoriasis-like dermatitis, Vγ4+ γδT17 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 γδT17 cells in this inflammatory condition.