Nonclassical CD1d-restricted NK T cells that produce IL-13 characterize an atypical Th2 response in ulcerative colitis.

By I. Fuss, F. Heller, M. Boirivant, F. León, Masaru Yoshida, S. Fichtner‐Feigl, Zhiqiong Yang, M. Exley, A. Kitani, R. Blumberg and 2 more. Journal of Clinical Investigation, 2004

801 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/fde979ead55de038cf13841268333445a6944541

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. R. Sartor
2. Q. Guan
3. W. Strober
4. A. Kitani
5. Takuya Suzuki
6. I. Junttila
7. E. Shevach

Citations in the corpus

• Innate and adaptive immunity in inflammatory bowel disease. (2014, background): “J Clin Invest [63] Positivity of αCD2/28-stim NK T cells FACS”
• Mechanisms of Disease: pathogenesis of Crohn's disease and ulcerative colitis (2006, result): “On the basis of results obtained from studies of the oxazalone colitis model, one of the few models to exhibit a T H 2 profile, Fuss and colleagues have suggested that ulcerative colitis has an atypical T H 2 response, mediated by natural killer T cells that secrete IL-13”
• A Comprehensive Review and Update on the Pathogenesis of Inflammatory Bowel Disease (2019, background): “IL-13, a key effector Th2 cytokine in ulcerative colitis, also shows the ability to impair epithelial barrier function by affecting epithelial apoptosis, tight junctions, and reconstitution velocity [57].”
• Regulation of intestinal epithelial permeability by tight junctions (2012, background): “It has been reported that IL-13 expression is elevated under inflammatory conditions, such as in the colonic mucosa of UC and CD patients [139, 140], and that this elevation possibly contributes to intestinal barrier dysfunction.”