Journal
CYTOKINE
Volume 100, Issue -, Pages 1-10Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2017.06.017
Keywords
Interleultin-33; Intestinal immunity; T cells; Inflammatory bowel disease; Microbiome
Funding
- National Institutes of Health - United States [K08DK101608, R03DK111473]
- March of Dimes Foundation - United States [5-FY17-79]
- Children's Discovery Institute of Washington University
- St. Louis Children's Hospital
- Department of Pediatrics at Washington University School of Medicine, St. Louis
- NIH [T32 GM07200]
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Interleukin-33 (IL-33) is a member of the IL-1 cytokine family that has been widely studied since its discovery in 2005 for its dichotomous functions in homeostasis and inflammation. IL-33, along with its receptor suppression of tumorigenicity 2 (ST2), has been shown to modulate both the innate and adaptive immune system. Originally, the IL-33/ST2 signaling axis was studied in the context of inducing type 2 immune responses with the expression of ST2 by T helper 2 (T(H)2) cells. However, the role of IL-33 is not limited to TH2 responses. Rather, IL-33 is a potent activator of T(H)1 cells, group 2 innate lymphoid cells (ILC2s), regulatory T (Treg) cells, and CD8(+) T cells. The intestine is uniquely important in this discussion, as the intestinal epithelium is distinctively positioned to interact with both pathogens and the immune cells housed in the mucosa. In the intestine, IL-33 is expressed by the pericryptal fibroblasts and its expression is increased particularly in disease states. Moreover, IL-33/ST2 signaling aberrancy is implicated in the pathogenesis of inflammatory bowel disease (IBD). Accordingly, for this review, we will focus on the role of IL-33 in the regulation of intestinal immunity, involvement in intestinal disease, and implication in potential therapeutics.
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