| First Author | St Leger AJ | Year | 2018 |
| Journal | J Exp Med | Volume | 215 |
| Issue | 4 | Pages | 1079-1090 |
| PubMed ID | 29490936 | Mgi Jnum | J:261600 |
| Mgi Id | MGI:6155878 | Doi | 10.1084/jem.20170369 |
| Citation | St Leger AJ, et al. (2018) STAT-3-independent production of IL-17 by mouse innate-like alphabeta T cells controls ocular infection. J Exp Med 215(4):1079-1090 |
| abstractText | Appropriate regulation of IL-17 production in the host can mean the difference between effective control of pathogens and uncontrolled inflammation that causes tissue damage. Investigation of conventional CD4(+) T cells (Th17 cells) has yielded invaluable insights into IL-17 function and its regulation. More recently, we and others reported production of IL-17 from innate alphabeta+ T cell populations, which was shown to occur primarily via IL-23R signaling through the transcription factor STAT-3. In our current study, we identify promyelocytic leukemia zinc finger (PLZF)-expressing iNKT, CD4(-)/CD8(+), and CD4(-)/CD8(-) (DN) alphabeta+T cells, which produce IL-17 in response to TCR and IL-1 receptor ligation independently of STAT-3 signaling. Notably, this noncanonical pathway of IL-17 production may be important in mucosal defense and is by itself sufficient to control pathogenic Staphylococcus aureus infection at the ocular surface. |
