Journal
FASEB JOURNAL
Volume 33, Issue 12, Pages 13951-13965Publisher
WILEY
DOI: 10.1096/fj.201901446R
Keywords
IL-23; pathogenic Th17 cells; IL-23R; GM-CSF; IL-22
Categories
Funding
- National Natural Science Foundation of China [81570834, 81770901, 81870675]
- Scientific Research Foundation for the Returned Overseas Chinese Scholars
- State Education Ministry [48]
- Tianjin Clinical Key Discipline Project [TJLCZDXKT003]
Ask authors/readers for more resources
Pathogenic T helper (T-h)17 cells are key mediators of autoimmune diseases such as uveitis and its animal model, experimental autoimmune uveitis (EAU). However, the contribution of microRNAs (miRs) to the intrinsic control of pathogenic T(h)17 cells in EAU remains largely unknown. Here, we have reported that miR-223-3p was significantly up-regulated in interphotoreceptor retinoid-binding protein specific Th17 cells, and its expression was enhanced by IL-23 signal transducer and activator of transcription 3 signaling. Knockdown of miR-223-3p decreased the pathogenicity of T(h)17 cells in a T-cell transfer model of EAU. Mechanistic studies showed that miR-2233-p directly repressed the expression of forkhead box 03 (FOXO3), and FOXO3 negatively regulated pathogenic Th17 cell responses partially via suppression of IL-23 receptor expression. Thus, our results reveal an important role for miR-223-3p in autoreactive T(h)17 cell responses and suggest a potential therapeutic avenue for uveitis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available