Open Access

MINI-REVIEW

Role of IL-33 in transplant biology

Ying Jin¹, Deqiang Kong², Chen Liu², Weihua Gong²

1 Zhejiang University, Second Affiliated Hospital of School of Medicine, Department of Traditional Chinese Medicine & Rehabilitation, Hangzhou City, People’s Republic of China
2 Zhejiang University, Second Affiliated Hospital of School of Medicine, Department of General Surgery, Hangzhou City, People’s Republic of China

* Corresponding Author: Weihua Gong,

European Cytokine Network 2019, 30(2), 39-42. https://doi.org/10.1684/ ecn.2019.0429

Accepted 28 March 2019;

Abstract

Since the pro-inflammatory cytokine IL-33 and its receptor (ST2) are closely involved in regulating both innate and adaptiveimmune responses,itis conceivable that theymay play animportant rolein organ transplantation. IL-33 is broadly expressed by multiple cell types such as fibroblasts, epithelial cells, and endothelial cells. As a strong inducer of type 2 helperT (Th2) cellularimmune responses, IL-33 can significantly prolong allograft survivalin organ transplantation partially via altering gene expression profiles and increasing frequency of regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs). Nevertheless, the IL-33 signaling pathway and its underlying mechanisms remain largely undefined in transplant biology. This present mini-review summarizes recent advances in the studies concerning the IL-33/ ST2 signaling pathway and the analysis of its biological function in the field transplantation. The literature points to a deleterious role of activation of the IL-33/ST2 signaling pathway, giving rise to ischemia/reperfusion, acute kidney injury and failure, acute heart rejection, as well as liver fibrosis. Under pro-inflammatory conditions, IL-33 expression is upregulated.Alteration of IL-33levels has been suggested as a biomarker for predicting organinjury and ongoing allogeneic transplant outcome. These studies have deepened our understanding of immunobiological role of IL-33 and its receptor in organ transplantation.Modulation of the IL-33/ST2 signaling pathwaymight be utilized as a therapeutic targetin theclinic.

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