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Rheumatoid arthritis

Who knows why regulatory T cells are defective in RA ... IDO

Nature Reviews Rheumatology volume 10, page 381 (2014)Cite this article

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“It has been known for a number of years that regulatory T (TREG) cells, which normally control excessive immune responses, are defective in patients with rheumatoid arthritis (RA),” says Richard Williams (Kennedy Institute, the University of Oxford) regarding the motivation for his new publication in the journal Arthritis & Rheumatology. His team of UK researchers has discovered that methylation of the CTLA4 promoter in TREG cells prevents antigen-presenting cells (APCs) from expressing indoleamine-pyrrole 2,3-dioxygenase (IDO). This epigenetic regulation of CTLA4 is thereby a mechanism to explain defective TREG-cell function in the pathogenesis of autoimmune diseases, such as RA.

TREG cells are thought to prevent the autoreactive T-cell-mediated inflammation that is characteristic of many autoimmune diseases. Patients with RA are known to have TREG cells with low surface expression of cytotoxic T lymphocyte protein 4 (CTLA-4), an inhibitory molecule that is vital for the direct cell–cell suppressive function of TREG cells. Low CTLA4 expression was therefore thought to be involved in the pathogenesis of synovial inflammation, but no mechanism for this defect had been defined, until now.

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References

  1. Cribbs, A.P. et al. Regulatory T cell function in rheumatoid arthritis is compromised by CTLA-4 promoter methylation resulting in a failture to activate the IDO pathway. Arthritis Rheum. 10.1002/art.38715

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  1. Nicholas J. Bernard
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Bernard, N. Who knows why regulatory T cells are defective in RA ... IDO. Nat Rev Rheumatol 10, 381 (2014). https://doi.org/10.1038/nrrheum.2014.96

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  • DOI: https://doi.org/10.1038/nrrheum.2014.96

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