| First Author | Kim TS | Year | 2024 |
| Journal | Immunity | Volume | 57 |
| Issue | 4 | Pages | 859-875.e11 |
| PubMed ID | 38513665 | Mgi Jnum | J:359559 |
| Mgi Id | MGI:7787194 | Doi | 10.1016/j.immuni.2024.02.020 |
| Citation | Kim TS, et al. (2024) Epithelial-derived interleukin-23 promotes oral mucosal immunopathology. Immunity 57(4):859-875.e11 |
| abstractText | At mucosal surfaces, epithelial cells provide a structural barrier and an immune defense system. However, dysregulated epithelial responses can contribute to disease states. Here, we demonstrated that epithelial cell-intrinsic production of interleukin-23 (IL-23) triggers an inflammatory loop in the prevalent oral disease periodontitis. Epithelial IL-23 expression localized to areas proximal to the disease-associated microbiome and was evident in experimental models and patients with common and genetic forms of disease. Mechanistically, flagellated microbial species of the periodontitis microbiome triggered epithelial IL-23 induction in a TLR5 receptor-dependent manner. Therefore, unlike other Th17-driven diseases, non-hematopoietic-cell-derived IL-23 served as an initiator of pathogenic inflammation in periodontitis. Beyond periodontitis, analysis of publicly available datasets revealed the expression of epithelial IL-23 in settings of infection, malignancy, and autoimmunity, suggesting a broader role for epithelial-intrinsic IL-23 in human disease. Collectively, this work highlights an important role for the barrier epithelium in the induction of IL-23-mediated inflammation. |
