| First Author | Zhang H | Year | 2019 |
| Journal | Cell Rep | Volume | 29 |
| Issue | 2 | Pages | 391-405.e5 |
| PubMed ID | 31597099 | Mgi Jnum | J:284783 |
| Mgi Id | MGI:6390061 | Doi | 10.1016/j.celrep.2019.09.003 |
| Citation | Zhang H, et al. (2019) CD109 Restrains Activation of Cutaneous IL-17-Producing gammadelta T Cells by Commensal Microbiota. Cell Rep 29(2):391-405.e5 |
| abstractText | Interleukin-17-producing gammadelta T (gammadelta17) cells play a central role in protective and pathogenic immune responses. However, the tissue-specific mechanisms that control the activation of these innate lymphocytes are not known. Here, we demonstrate that CD109, a glycosylphosphatidylinositol (GPI)-anchored protein highly expressed by keratinocytes, is an important regulator of skin homeostasis and gammadelta17 cell activation. Genetic deletion of CD109 results in spontaneous epidermal hyperplasia, aberrant accumulation of dermal-derived gammadelta17 cells, and enhanced susceptibility to psoriasiform inflammation. In this context, gammadelta17 activation requires interleukin (IL)-23 signals and is reversed by transient depletion of the skin microbiota. Mechanistically, CD109 restrains gammadelta17 cell activation in a cell-extrinsic manner by fortifying skin barrier integrity. Collectively, our data provide insight into the regulation of the skin IL-23/IL-17 immune axis and how homeostasis is maintained at this important barrier site. |
