Dual immune functions of IL-33 in inflammatory bowel disease

• Jie Chen ^[1] ; Yan He ^[2] ; Lei Tu ^[3] ; Lihua Duan ^[1]
  1. [1] Nanchang University

     Nanchang University

     China

     
  2. [2] First Affiliated Hospital of Xiamen University

     First Affiliated Hospital of Xiamen University

     China

     
  3. [3] Huazhong University of Science and Technology

     Huazhong University of Science and Technology

     China

     

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• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 35, Nº. 2, 2020, págs. 137-146
• Idioma: inglés
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• Resumen

  • Interleukin-33 (IL-33) has emerged as a critical regulator in a variety of diseases, including inflammatory bowel disease (IBD). IL-33 can be produced by various tissues and cells, and typically induces Th2-type immune responses via binding to the receptor ST2. In addition, accumulated data have shown that IL-33 also plays a modulatory role in the function of regulatory T cells (Tregs), B cells, and innate immune cells such as macrophages and innate lymphoid cells (ILCs). IBD, including Crohn’s disease and ulcerative colitis, are characterized by aberrant immunological responses leading to intestinal tissue injury and destruction. Although IL-33 expression is increased in IBD patients and correlates with the patients’ disease activity index, mechanistic studies to date have demonstrated both pathogenic and protective roles in animal models of experimental colitis. In this review, we will summarize the roles and mechanisms of IL-33 in IBD, which is essential to understand the pathogenesis of IBD and determine potential therapies.