| First Author | Gray EE | Year | 2013 |
| Journal | Nat Immunol | Volume | 14 |
| Issue | 6 | Pages | 584-92 |
| PubMed ID | 23624556 | Mgi Jnum | J:197335 |
| Mgi Id | MGI:5492191 | Doi | 10.1038/ni.2585 |
| Citation | Gray EE, et al. (2013) Deficiency in IL-17-committed Vgamma4(+) gammadelta T cells in a spontaneous Sox13-mutant CD45.1(+) congenic mouse substrain provides protection from dermatitis. Nat Immunol 14(6):584-92 |
| abstractText | Interleukin 17 (IL-17)-committed gammadelta T cells (gammadeltaT17 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 Vgamma4(+) gammadeltaT17 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 gammadeltaT17 cells migrated from skin to lymph nodes at low rates. In a model of psoriasis-like dermatitis, the Vgamma4(+) gammadeltaT17 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 gammadeltaT17 cells in this inflammatory condition. |
