| First Author | McKenzie DR | Year | 2022 |
| Journal | Nat Immunol | Volume | 23 |
| Issue | 3 | Pages | 411-422 |
| PubMed ID | 35165446 | Mgi Jnum | J:323863 |
| Mgi Id | MGI:7264838 | Doi | 10.1038/s41590-021-01124-8 |
| Citation | McKenzie DR, et al. (2022) Normality sensing licenses local T cells for innate-like tissue surveillance. Nat Immunol 23(3):411-422 |
| abstractText | The increasing implication of lymphocytes in general physiology and immune surveillance outside of infection poses the question of how their antigen receptors might be involved. Here, we show that macromolecular aggregates of intraepidermal gammadelta T cell antigen receptors (TCRs) in the mouse skin aligned with and depended on Skint1, a butyrophilin-like (BTNL) protein expressed by differentiated keratinocytes (KCs) at steady state. Interruption of TCR-mediated 'normality sensing' had no impact on gammadelta T cell numbers but altered their signature phenotype, while the epidermal barrier function was compromised. In addition to the regulation of steady-state physiology, normality sensing licensed intraepidermal T cells to respond rapidly to subsequent tissue perturbation by using innate tumor necrosis factor (TNF) superfamily receptors. Thus, interfering with Skint1-dependent interactions between local gammadelta T cells and KCs at steady state increased the susceptibility to ultraviolet B radiation (UVR)-induced DNA damage and inflammation, two cancer-disposing factors. |
