Sopping up IL-22 drives intestinal disease

Mucosal Immunity The causes of inflammatory bowel disease (IBD) such as Crohn's disease and ulcerative colitis are likely complex and multifactorial, involving loss of epithelial cell integrity, chronic inflammation, and changes to the microbiota. Pelczar et al. investigated potential disease-driving mechanisms by studying IBD patients and mouse models. IBD patients express elevated levels of interleukin-22 binding protein (IL-22BP), which binds to the protein IL-22, preventing its tissue repair–promoting actions. Moreover, IBD development in mouse models requires IL-22BP. Lastly, IBD patients responding to therapy with antibodies against tumor necrosis factor–α exhibited reduced levels of IL-22BP but retained IL-22 expression, suggesting one mechanism by which this therapy may act. ![Figure][1] Illustration of an abnormal growth and inflammation in bowel disease PHOTO: SPRINGER MEDIZIN/SCIENCE SOURCE Science , this issue p. [358][2] [1]: pending:yes [2]: /lookup/doi/10.1126/science.aah5903