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Curr Rheumatol Rep. 2013 Sep;15(9):352. doi: 10.1007/s11926-013-0352-0.

Treg cells in rheumatoid arthritis: an update.

Author information

1
Newcastle NIHR Biomedical Research Centre at Newcastle upon Tyne Hospitals NHS Foundation Trust and Newcastle University, Newcastle upon Tyne, UK. faye.cooles@ncl.ac.uk

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease arising from a breakdown in immunological self-tolerance, which leads to aberrant immune responses to autoantigens. Regulatory CD4(+) T-cells (Tregs) underpin one of the key mechanisms of self-tolerance and are a major focus of study in RA and other autoimmune diseases. In order to design new and improved therapies to reinstate self-tolerance, and perhaps cure disease, we need to understand the complex mechanism of action of Tregs. This review addresses recent findings in the field of Tregs in RA, with particular focus on identification of potential defects in Treg-mediated self-tolerance mechanisms present in RA patients, as well as how Tregs interact with other cells in the inflamed joints. As antigen-specific Tregs are a potential route for the reinstatement of immune tolerance, we also discuss new strategies currently being investigated which expand or induce de novo generation of Tregs.

PMID:
23888361
DOI:
10.1007/s11926-013-0352-0
[Indexed for MEDLINE]

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