@Article{ecn.2019.0429,
AUTHOR = {Ying Jin, Deqiang Kong, Chen Liu, Weihua Gong},
TITLE = {Role of IL-33 in transplant biology},
JOURNAL = {European Cytokine Network},
VOLUME = {30},
YEAR = {2019},
NUMBER = {2},
PAGES = {39--42},
URL = {http://www.techscience.com/ECN/v30n2/65393},
ISSN = {1952-4005},
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.},
DOI = {10.1684/ ecn.2019.0429}
}