Innate and adaptive interleukin-22 protects mice from inflammatory bowel disease

By Lauren A. Zenewicz, G. Yancopoulos, D. Valenzuela, A. Murphy, S. Stevens, R. Flavell. Immunity, 2008

859 citations recorded by the source corpus.

Inflammatory bowel disease (IBD) is a chronic inflammatory disease thought to be mediated by dysfunctional innate and/or adaptive immunity. This aberrant immune response leads to the secretion of harmful cytokines that destroy the epithelium of the gastrointestinal tract leading to further inflammation. IL-22 is a Th17 T cell associated cytokine that is bi-functional with both pro-inflammatory and protective effects on tissues depending on the inflammatory context. We show herein that IL-22 protects mice from IBD. Interestingly, this protection is not only mediated by CD4 T cells, but IL-22 expressing NK cells also confer protection. In addition, IL-22 expression is differentially regulated between NK cell subsets. Thus, both the innate and adaptive immune responses have developed protective mechanisms to counteract the damaging effects of inflammation on tissues.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/2e11aa79e4b4017a873f5cdd67af5f71a1e44dfc

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Citations in the corpus

Progressive loss of RORγt expression confers distinct functional fates to natural killer cell receptor-expressing RORγt+ innate lymphocytes (2010, neutral): “In mice, these cells are involved in safeguarding epithelial homeostasis (Sanos et al., 2009) and in protecting against various forms of experimental colitis (Satoh-Takayama et al., 2008; Zenewicz et al., 2008).”
Production of interleukin 22 but not interleukin 17 by a subset of human skin-homing memory T cells (2009, background): “IL-22 is a cytokine of the IL-10 family produced by T H -17 cells and the NK-22 subset of natural killer cell”
STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing (2009, background): “Among those lines, NK cells have recently been established as producers of IL-22 and some NK cell populations express CD11c (Zenewicz et al., 2008).”
IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine (2012, positive): “First we showed, by the administration of neutralizing IL-22 antibody, that IL-22 is protective during the peak of disease, but detrimental during the recovery phase (Supplemental Figure 9).”
The NLRP3 inflammasome protects against loss of epithelial integrity and mortality during experimental colitis (2010, neutral): “In addition to IL-18, the cytokines IL-11 and IL-22 have been identified as important regulators of Immunity 32, 379–391, March 26, 2010 ª2010 Elsevier Inc. 387 gastrointestinal mucosal biology (Keith et al., 1994; Zenewicz et al., 2008).”
The Microbiome in Infectious Disease and Inflammation (2012, neutral): “of experimental colitis by safeguarding epithelial homeostasis (204).”
RORγt+ innate lymphoid cells regulate intestinal homeostasis by integrating negative signals from the symbiotic microbiota (2011, background): “14 ) and, as a possible consequence, protects colon and hepatocytes from acute inflammatio”