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Immunologic Research
Published in: Immunologic Research 2-3/2019

01-06-2019 | Arterial Occlusive Disease | Review

RGC-32 and diseases: the first 20 years

Authors: Sonia I. Vlaicu, Alexandru Tatomir, Freidrich Anselmo, Dallas Boodhoo, Romeo Chira, Violeta Rus, Horea Rus

Published in: Immunologic Research | Issue 2-3/2019

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Abstract

The response gene to complement (RGC)-32 acts as a cell cycle regulator and mediator of TGF-β effects. However, recent studies have revealed other functions for RGC-32 in diverse processes such as cellular migration, differentiation, and fibrosis. In addition to its induction by complement activation and the C5b-9 terminal complement complex, RGC-32 expression is also stimulated by growth factors, hormones, and cytokines. RGC-32 is induced by TGF-β through Smad3 and RhoA signaling and plays an important role in cell differentiation. In particular, RGC-32 is essential for the differentiation of Th17 cells. RGC-32−/− mice display an attenuated experimental autoimmune encephalomyelitis phenotype that is accompanied by decreased central nervous system inflammation and reductions in IL-17- and GM-CSF-producing CD4+ T cells. Accumulating evidence has drawn attention to the deregulated expression of RGC-32 in human cancers, atherogenesis, metabolic disorders, and autoimmune disease. Furthermore, RGC-32 is a potential therapeutic target in multiple sclerosis and other Th17-mediated autoimmune diseases. A better understanding of the mechanism(s) by which RGC-32 contributes to the pathogenesis of all these diseases will provide new insights into its therapeutic potential.
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Metadata
Title
RGC-32 and diseases: the first 20 years
Authors
Sonia I. Vlaicu
Alexandru Tatomir
Freidrich Anselmo
Dallas Boodhoo
Romeo Chira
Violeta Rus
Horea Rus
Publication date
01-06-2019
Publisher
Springer US
Published in
Immunologic Research / Issue 2-3/2019
Print ISSN: 0257-277X
Electronic ISSN: 1559-0755
DOI
https://doi.org/10.1007/s12026-019-09080-0

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