Department of Medicine and Program in Biomedical Sciences, UCSD School of Medicine, La Jolla, California, USA.
Address correspondence to: Kim E. Barrett, Mailcode 0063, UCSD, 9500 Gilman Drive, La Jolla, California 92093-0063, USA. Phone: 858.534.2796; Email: email@example.com.
First published August 24, 2020 - More info
The tight junction protein claudin-2 is upregulated in inflammatory bowel disease, and yet its deficit worsens infectious and chemical colitis. In this issue of the JCI, Raju and Shashikanth et al. examined the contribution of claudin-2 to immune-mediated colitis. The authors used transgenic mouse models to show that claudin-2 deficiency attenuated colitis progression as well as a leak barrier defect, albeit at the risk of intestinal obstruction. Further, inhibition of claudin-2 by targeting casein kinase 2 (CK2) also ameliorated colitis. The findings reveal unsuspected links between the pore and leak pathways of intestinal permeability and immune responses leading to colitis. They additionally suggest potential targets for therapeutic intervention in inflammatory bowel disease.
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