Movatterモバイル変換

[0]ホーム
URL:

Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
Thehttps:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

NIH NLM Logo
Log inShow account info
Access keysNCBI HomepageMyNCBI HomepageMain ContentMain Navigation
pubmed logo
Advanced Clipboard
User Guide

Full text links

Frontiers Media SA full text link Frontiers Media SA Free PMC article
Full text links

Actions

Share

Review
.2015 Jul 14:6:236.
doi: 10.3389/fgene.2015.00236. eCollection 2015.

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

Affiliations
Review

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

Deena Khan et al. Front Genet..

Abstract

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, RORγt, 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.

Keywords: autoimmune; inflammation; interleukin 17; microRNA; transcription.

PubMed Disclaimer

Figures

FIGURE 1
FIGURE 1
Positive and negative transcriptional tegulators of IL-17 induction: Different cytokines and antigen specific stimuli trigger (black arrows and lines) different signaling cascades for activation ofRORc and consequentlyIl17 gene. Negative regulators (red arrows and lines), T-bet or FoxP3 interaction with RUNX1 prevents RORγt-RUNX1 interaction, which prevents RORγt-mediated IL-17 induction. Def6 binding to IRF4 prevents ROCK2-mediated IRF4 phosphorylation and subsequent IL-17 induction. PPARγ, peroxisome proliferator activated receptor γ; SOCS, suppressors of cytokine signaling; TCR, T cell receptor; BATF, B cell-activating transcription factor; IL, interleukin; TGFβ, transforming growth factor β; RORγt, retinoic acid-related orphan receptor γt; STAT, signal transducer and activator of transcription; IRF-4, interferon-inducible factor-4; RUNX1, Runt-related transcription factor 1; IRAK, IL-1 receptor-associated kinase; TRAF6, TNF receptor associated factor-6; ROCK, Rho-associated serine/threonine kinases.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Acosta-Rodriguez E. V., Napolitani G., Lanzavecchia A., Sallusto F. (2007). Interleukins 1beta and 6 but not transforming growth factor-beta are essential for the differentiation of interleukin 17-producing human T helper cells. Nat. Immunol. 8 942–949. 10.1038/ni1496 - DOI - PubMed
    1. Aggarwal S., Ghilardi N., Xie M. H., de Sauvage F. J., Gurney A. L. (2003). Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17. J. Biol. Chem. 278 1910–1914. 10.1074/jbc.M207577200 - DOI - PubMed
    1. An J., Golech S., Klaewsongkram J., Zhang Y., Subedi K., Huston G. E., et al. (2011). Kruppel-like factor 4 (KLF4) directly regulates proliferation in thymocyte development and IL-17 expression during Th17 differentiation. FASEB J. 25 3634–3645. 10.1096/fj.11-186924 - DOI - PMC - PubMed
    1. Andoh A., Takaya H., Makino J., Sato H., Bamba S., Araki Y., et al. (2001). Cooperation of interleukin-17 and interferon-gamma on chemokine secretion in human fetal intestinal epithelial cells. Clin. Exp. Immunol. 125 56–63. 10.1046/j.1365-2249.2001.01588.x - DOI - PMC - PubMed
    1. Arisawa T., Tahara T., Shiroeda H., Matsue Y., Minato T., Nomura T., et al. (2012). Genetic polymorphisms of IL17A and pri-microRNA-938, targeting IL17A 3′-UTR, influence susceptibility to gastric cancer. Hum. Immunol. 73 747–752. 10.1016/j.humimm.2012.04.011 - DOI - PubMed

Publication types

Related information

LinkOut - more resources

Full text links
Frontiers Media SA full text link Frontiers Media SA Free PMC article
Cite
Send To

NCBI Literature Resources

MeSHPMCBookshelfDisclaimer

The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). Unauthorized use of these marks is strictly prohibited.

[8]ページ先頭
©2009-2025 Movatter.jp