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

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015:2015:751793.
doi: 10.1155/2015/751793. Epub 2015 Mar 30.

Altered immunoregulation in rheumatoid arthritis: the role of regulatory T cells and proinflammatory Th17 cells and therapeutic implications

Affiliations
Review

Altered immunoregulation in rheumatoid arthritis: the role of regulatory T cells and proinflammatory Th17 cells and therapeutic implications

Alessia Alunno et al. Mediators Inflamm. 2015.

Abstract

In recent years several studies investigated the role of T lymphocyte subpopulations in the pathogenesis of rheumatoid arthritis (RA). Pathogenic Th17 cells mediate pannus growth, osteoclastogenesis, and synovial neoangiogenesis; hence they are key players in the development of the disease. On the other hand, regulatory T (Treg) cells are a T cell subset whose peculiar function is to suppress autoreactive lymphocytes. The imbalance between Th17 and Treg cells has been identified as a crucial event in the pathogenesis of RA. In addition, the effects of currently employed RA therapeutic strategies on these lymphocyte subpopulations have been extensively investigated. This review article aims to discuss current knowledge on Treg and Th17 cells in RA and possible implications of their therapeutic targeting in this disorder.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Therapeutic targeting of Treg and Th17 cells in rheumatoid arthritis (RA). The figure displays currently employed therapeutic approaches in RA for which an effect on Treg and Th17 cells has been reported in the literature (see text for details). Other compounds depicted in the figure are currently under investigation in RA or have been tested in experimental models of the disease. CTLA-4: cytotoxic T lymphocyte antigen 4; IL: interleukin; TGF-β: transforming growth factor-β; TNF: tumor necrosis factor.

References

    1. McInnes I. B., Schett G. The pathogenesis of rheumatoid arthritis. The New England Journal of Medicine. 2011;365(23):2205–2219. doi: 10.1056/nejmra1004965. - DOI - PubMed
    1. Wells A. U., Denton C. P. Interstitial lung disease in connective tissue disease—mechanisms and management. Nature Reviews Rheumatology. 2014;10(12):728–739. doi: 10.1038/nrrheum.2014.149. - DOI - PubMed
    1. Turesson C. Extra-articular rheumatoid arthritis. Current Opinion in Rheumatology. 2013;25(3):360–366. doi: 10.1097/bor.0b013e32835f693f. - DOI - PubMed
    1. Gizinski A. M., Fox D. A. T cell subsets and their role in the pathogenesis of rheumatic disease. Current Opinion in Rheumatology. 2014;26(2):204–210. doi: 10.1097/BOR.0000000000000036. - DOI - PubMed
    1. O'Shea J., Paul W. E. Mechanisms underlying lineage commitment and plasticity of helper CD4+ T cells. Science. 2010;327(5969):1098–1102. doi: 10.1126/science.1178334. - DOI - PMC - PubMed

MeSH terms