Switching off a “danger sensor” on immune cells prevents inflammation in a model of Rheumatoid Arthritis

Publication of the DRFZ at the Journal of Experimental Medicine: Chiara Romagnani and colleagues have discovered a new target for the treatment of Rheumatoid Arthritis and other chronic inflammations. They were able to hamper the development of arthritis in an animal model by switching off the “danger sensor” NKG2D selectively in immune cells, the T-helper cells, which play a pathogenic role in the disease. By switching off NKG2D, production of pro-inflammatory cytokines by T-helper cells was impaired and resulted in reduced tissue inflammation and amelioration of disease severity.