Phosphorylation of Regnase-1 lets IL-17 run amok

When considering the role of the key immune molecule interleukin (IL)-17, the phrase "too much of a good thing" springs to mind. Because unlike some of its more sedate cytokine cousins which studiously direct the immune response to destroy invading pathogens, IL-17 can get a little carried away. So much so that excess inflammation caused by IL-17 has been implicated in autoimmune disorders such as rheumatoid arthritis, psoriasis, and multiple sclerosis.

* This article was originally published here