Deficiency in IL-17-committed V?4(+) ?? T cells in a spontaneous Sox13-mutant CD45.1(+) congenic mouse substrain provides protection from dermatitis.

ABSTRACT: Interleukin 17 (IL-17)-committed ?? T cells (??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?4(+) ??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 ??T17 cells migrated from skin to lymph nodes at low rates. In a model of psoriasis-like dermatitis, the V?4(+) ??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 ??T17 cells in this inflammatory condition.

SUBMITTER: Gray EE 

PROVIDER: S-EPMC3660499 | biostudies-literature | 2013 Jun

REPOSITORIES: biostudies-literature