1. STAT-3-independent production of IL-17 by mouse innate-like αβ T cells controls ocular infection.
- Author
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St Leger AJ, Hansen AM, Karauzum H, Horai R, Yu CR, Laurence A, Mayer-Barber KD, Silver P, Villasmil R, Egwuagu C, Datta SK, and Caspi RR
- Subjects
- Animals, Immunologic Memory, Interleukins metabolism, Mice, Inbred C57BL, Mice, Knockout, Mucous Membrane immunology, Mucous Membrane microbiology, Nuclear Receptor Subfamily 1, Group F, Member 3 metabolism, Phosphorylation, Promyelocytic Leukemia Zinc Finger Protein metabolism, Signal Transduction, Staphylococcus aureus physiology, T-Lymphocytes metabolism, Th17 Cells metabolism, Thymus Gland metabolism, Eye Infections immunology, Eye Infections pathology, Immunity, Innate, Interleukin-17 biosynthesis, Receptors, Antigen, T-Cell, alpha-beta metabolism, STAT3 Transcription Factor metabolism
- Abstract
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 αβ+ 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) αβ+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., (This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply.)- Published
- 2018
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