IL-17 in pancreatic disease: pathogenesis and pharmacotherapy.
Am J Cancer Res
; 10(11): 3551-3564, 2020.
Article
in En
| MEDLINE
| ID: mdl-33294254
ABSTRACT
Increasing evidence highlights the role of the interleukin (IL)-17 family in pancreatic diseases. IL-17A induces acinar cell injury directly, recruits neutrophils, and cooperates with other inflammatory factors to exacerbate pancreatic inflammation. It also triggers islet ß-cell apoptosis and nitric oxide-dependent cytotoxicity, thus aggravating islet inflammation. IL-17A seems to have different roles in pancreatic intraepithelial neoplasia (PanIN) and pancreatic cancer (PC). IL-17A participates in the progression of acinar-ductal metaplasia (ADM) and PanIN, but not related to the characteristics of PC stem cells and the overall survival of patients. Acting similar to IL-17A, IL-17B accelerates the invasion and metastasis of PC, and predicts prognosis of PC and the therapeutic effect of gemcitabine. Herein, we review the current understanding of the pathogenesis of IL-17 in pancreatitis, type 1 diabetes mellitus (T1DM), and PC, as well as potential pharmacotherapy targeting IL-17 and its receptors in pancreatic diseases. The findings summarized in this article are of considerable significance for understanding the essential role of IL-17 in pancreatic diseases.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Type of study:
Etiology_studies
/
Prognostic_studies
Language:
En
Journal:
Am J Cancer Res
Year:
2020
Document type:
Article
Affiliation country: