From the Cover: CD39 deletion exacerbates experimental murine colitis and human polymorphisms increase susceptibility to inflammatory bowel disease.

@article{Friedman2009FromTC,
  title={From the Cover: CD39 deletion exacerbates experimental murine colitis and human polymorphisms increase susceptibility to inflammatory bowel disease.},
  author={David J. Friedman and Beat Martin K{\"u}nzli and Yousif I. A-Rahim and Jean S{\'e}vigny and Pascal O. Berberat and Keiichi Enjyoji and Eva Csizmadia and Helmut Friess and Simon Christopher Robson},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2009},
  volume={106 39},
  pages={16788-93}
}
CD39/ENTPD1 hydrolyzes proinflammatory nucleotides to generate adenosine. As purinergic mediators have been implicated in intestinal inflammation, we hypothesized that CD39 might protect against inflammatory bowel disease. We studied these possibilities in a mouse model of colitis using mice with global CD39 deletion. We then tested whether human genetic polymorphisms in the CD39 gene might influence susceptibility to Crohn's disease. We induced colitis in mice using Dextran Sodium Sulfate (DSS… CONTINUE READING

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