| First Author | Liu H | Year | 2017 |
| Journal | Cell Host Microbe | Volume | 22 |
| Issue | 5 | Pages | 653-666.e5 |
| PubMed ID | 29120743 | Mgi Jnum | J:278147 |
| Mgi Id | MGI:6284884 | Doi | 10.1016/j.chom.2017.10.006 |
| Citation | Liu H, et al. (2017) Staphylococcus aureus Epicutaneous Exposure Drives Skin Inflammation via IL-36-Mediated T Cell Responses. Cell Host Microbe 22(5):653-666.e5 |
| abstractText | Staphylococcus aureus colonization contributes to skin inflammation in diseases such as atopic dermatitis, but the signaling pathways involved are unclear. Herein, epicutaneous S. aureus exposure to mouse skin promoted MyD88-dependent skin inflammation initiated by IL-36, but not IL-1alpha/beta, IL-18, or IL-33. By contrast, an intradermal S. aureus challenge promoted MyD88-dependent host defense initiated by IL-1beta rather than IL-36, suggesting that different IL-1 cytokines trigger MyD88 signaling depending on the anatomical depth of S. aureus cutaneous exposure. The bacterial virulence factor PSMalpha, but not alpha-toxin or delta-toxin, contributed to the skin inflammation, which was driven by IL-17-producing gammadelta and CD4(+) T cells via direct IL-36R signaling in the T cells. Finally, adoptive transfer of IL-36R-expressing T cells to IL-36R-deficient mice was sufficient for mediating S. aureus-induced skin inflammation. Together, this study defines a previously unknown pathway by which S. aureus epicutaneous exposure promotes skin inflammation involving IL-36R/MyD88-dependent IL-17 T cell responses. |
