IMR Press / FBE / Volume 4 / Issue 4 / DOI: 10.2741/e474

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Review

MicroRNAs and other mechanisms regulate interleukin-17 cytokines and receptors

Show Less
1 Department of Pharmacology and Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA

*Author to whom correspondence should be addressed.

 

Front. Biosci. (Elite Ed) 2012, 4(4), 1478–1495; https://doi.org/10.2741/e474
Published: 1 January 2012
Abstract

Interleukin-17 cytokines are a family of proinflammatory cytokines. Our current studies found: i) IL17 cytokines are not ubiquitously expressed, but several receptors and TRAF3IP2 are ubiquitously expressed in tissues with a few exceptions; ii) heart and vascular tissue are in the second tier of readiness to respond to IL-17 cytokine stimulation; iii) alternative transcription starting sites and alternative spliced isoforms are found in IL-17 cytokine and receptor transcripts; iv) higher hypomethylation status is associated with higher expressions of IL-17 receptors; v) the binding sites of several RNA binding proteins are found in the 3’UTRs of the mRNAs of IL-17 cytokines and receptors; and vi) numerous microRNA binding sites are statistically equivalent to that of experimentally verified microRNAsmRNA interactions in the 3’UTRs of IL-17 cytokine and receptor mRNAs. These results suggest that mechanisms including alternative promoters, alternative splicing, RNA binding proteins, and microRNAs regulate the structures and expressions of IL-17 cytokines and receptors. These results provide an insight into the roles of IL-17 in mediating inflammation and immunity.

Keywords
interleukin-17 Cytokines
Interleukin-17 Receptors
Gene Expression
mRNA Stability
Vascular Inflammation
Review
Share
Back to top