HISTOLOGY AND HISTOPATHOLOGY

From Cell Biology to Tissue Engineering

 

Review

Dual immune functions of IL-33 in inflammatory bowel disease

Jie Chen1, Yan He2, Lei Tu3 and Lihua Duan4

1Department of Scientific Research and Education, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, Nanchang, 2Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, 3Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei and 4Department of Rheumatology and Clinical Immunology, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, Nanchang, China
*Jie Chen and Yan He have contributed equally to this work.

Offprint requests to: Dr. Lihua Duan, 92 Aiguo Road, Department of Rheumatology and Clinical Immunology, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, Nanchang, 330006, China. e-mail: lh-duan@163.com or Dr. Lei Tu, Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. e-mail: tulei_1985@126.com


Summary. 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. Histol Histopathol 35, 137-146 (2020)

Key words: Interleukin-33, Inflammatory bowel disease, ST2, Innate immune, Adaptive immune

DOI: 10.14670/HH-18-149