Molecular Mechanisms Underlying IL-33-Mediated Inflammation in Inflammatory Bowel Disease

被引:16
|
作者
Aggeletopoulou, Ioanna [1 ]
Tsounis, Efthymios P. P. [1 ]
Triantos, Christos [1 ]
机构
[1] Univ Hosp Patras, Dept Internal Med, Div Gastroenterol, GR-26504 Patras, Greece
关键词
intereukin-33; ST2; receptor; Crohn's disease; ulcerative colitis; inflammatory bowel disease; pathogenesis; AMELIORATES EXPERIMENTAL COLITIS; ULCERATIVE-COLITIS; IL-33; PROMOTES; INTERLEUKIN-33; CYTOKINE; INNATE; RECEPTOR; IMMUNITY; CELLS; EXPRESSION;
D O I
10.3390/ijms24010623
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Interleukin-33 (IL-33) is a cytokine defined by its pleiotropic function, acting either as a typical extracellular cytokine or as a nuclear transcription factor. IL-33 and its receptor, suppression of tumorigenicity 2 (ST2), interact with both innate and adaptive immunity and are considered critical regulators of inflammatory disorders. The IL-33/ST2 axis is involved in the maintenance of intestinal homeostasis; on the basis of their role as pro- or anti-inflammatory mediators of first-line innate immunity, their expression is of great importance in regard to mucosal defenses. Mucosal immunity commonly presents an imbalance in inflammatory bowel disease (IBD). This review summarizes the main cellular and molecular aspects of IL-33 and ST2, mainly focusing on the current evidence of the pro- and anti-inflammatory effects of the IL-33/ST2 axis in the course of ulcerative colitis and Crohn's disease, as well as the molecular mechanisms underlying the association of IL-33/ST2 signaling in IBD pathogenesis. Although IL-33 modulates and impacts the development, course, and recurrence of the inflammatory response, the exact role of this molecule is elusive, and it seems to be associated with the subtype of the disease or the disease stage. Unraveling of IL-33/ST2-mediated mechanisms involved in IBD pathology shows great potential for clinical application as therapeutic targets in IBD treatment.
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页数:12
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