Autoimmune disorders, including rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), occur when an individual's immune system turns on other cells in the body. Inappropriate and excessive production of the soluble immune mediators IL-17 and IL-21 have been linked to several autoimmune disorders. Understanding the molecular mechanisms underlying this aberrant production might identify new therapeutic targets.

A team of researchers, led by Alessandra Pernis, at Columbia University, New York, has now generated data in mice indicating that the protein ROCK2 might be a good therapeutic target in this context. A key piece of evidence to support this idea was the observation that administration of a ROCK inhibitor to mice with spontaneous disease that models either RA or SLE, decreased production of IL-17 and IL-21 and ameliorated disease symptoms.

Phosphorylation of IRF4 by ROCK2 regulates IL-17 and IL-21 production and the development of autoimmunity in mice

Karen Honey
Journal of Clinical Investigation