Regulation of IL-17 in autoimmune diseases by transcriptional factors and microRNAs

被引:56
作者
Khan, Deena [1 ]
Ahmed, S. Ansar [1 ]
机构
[1] Virginia Polytech Inst & State Univ, Virginia Maryland Coll Vet Med, Dept Biomed Sci & Pathobiol, Blacksburg, VA 24060 USA
来源
FRONTIERS IN GENETICS | 2015年 / 6卷
关键词
ROR-GAMMA-T; GROWTH-FACTOR-BETA; TH17; CELLS; TGF-BETA; INTERFERON-GAMMA; CUTTING EDGE; DECREASED EXPRESSION; RHEUMATOID-ARTHRITIS; MULTIPLE-SCLEROSIS; IL-23; RECEPTOR;
D O I
10.3389/fgene.2015.00236
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
In recent years, IL-17A (IL-17), a pro-inflammatory cytokine, has received intense attention of researchers and clinicians alike with documented effects in inflammation and autoimmune diseases. IL-17 mobilizes, recruits and activates different cells to increase inflammation. Although protective in infections, overproduction of IL-17 promotes inflammation in autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, psoriasis, among others. Regulating IL-17 levels or action by using IL-17-blocking antibodies or IL-17R antagonist has shown to attenuate experimental autoimmune diseases. It is now known that in addition to IL-17-specific transcription factor, ROR gamma t, several other transcription factors and select microRNAs (miRNA) regulate IL-17. Given that miRNAs are dysregulated in autoimmune diseases, a better understanding of transcriptional factors and miRNA regulation of IL-17 expression and function will be essential for devising potential new therapies. In this review, we will overview IL-17 induction and function in relation to autoimmune diseases. In addition, current findings on transcriptional regulation of IL-17 induction and plausible interplay between IL-17 and miRNA in autoimmune diseases are highlighted.
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页数:9
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