The I’s have it

A Science study has revealed that anti-inflammatory drugs targeting tumor necrosis factor α (TNFα) work in part by downregulating interleukin-22 receptor subunit alpha 2 (IL22RA2; IL-22BP) to increase IL-22 activity. The findings not only suggest the binding protein could serve as a biomarker of response to marketed therapies but validate the approach of developing IL-22, and raise the possibility of developing inhibitors of IL22RA2 as an alternative.

Although anti-TNFs are commonly used to treat a variety of autoimmune and inflammatory diseases, their mechanisms of action are complex and not fully understood...