TH17 Cells Convert From Pro-Inflammatory to Anti-Inflammatory

Possible Therapeutic Strategy for Inflammation-Mediated Diseases

Yale researchers found that TH17 cells can switch from a pro-inflammatory state to a regulatory cell that limits inflammation, based on mouse model experiments.

New research shows that TH17 cells can convert from pro-inflammatory to anti-inflammatory, revealing a possible therapeutic strategy for inflammation-mediated diseases.

A type of immune cell that promotes inflammation during the immune response, TH17, can convert into another type of cell that reduces inflammation, Yale researchers have found. The finding, published on April 29 in the journal Nature, points to a possible therapeutic strategy for inflammation-mediated diseases, such as inflammatory bowel disease, multiple sclerosis, and rheumatoid arthritis.

The research team, led by Yale’s chair of immunobiology, Dr. Richard Flavell, used mouse models to observe TH17 cells, which have been known to change behavior when stimulated. Through a series of experiments, they found that the TH17 cells that had expressed a pro-inflammatory response had converted into a regulatory cell with the ability to limit inflammation.

This conversion from pro-inflammatory to anti-inflammatory is an example of “transdifferentiation,” a process of reprogramming from one type of immune cell to a completely different type. TH17’s ability to transdifferentiate suggests that it may be a target for the development of future immunotherapies without the negative side effects of current immunosuppressive treatments, say the researchers.

Reference: “Th17 cells transdifferentiate into regulatory T cells during resolution of inflammation” by Nicola Gagliani, Maria Carolina Amezcua Vesely, Andrea Iseppon, Leonie Brockmann, Hao Xu, Noah W. Palm, Marcel R. de Zoete, Paula Licona-Limón, Ricardo S. Paiva, Travers Ching, Casey Weaver, Xiaoyuan Zi, Xinghua Pan, Rong Fan, Lana X. Garmire, Matthew J. Cotton, Yotam Drier, Bradley Bernstein, Jens Geginat, Brigitta Stockinger, Enric Esplugues, Samuel Huber and Richard A. Flavell, 29 April 2015, Nature.
DOI: 10.1038/nature14452

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