Qin, Shan-yu, Lu, Dong-hong, Guo, Xiao-yun, Luo, Wei, Hu, Bang-li, Huang, Xiao-li, Chen, Mei, Wang, Jia-xu, Ma, Shi-Jia, Yang, Xian-wen, Jiang, Hai-xing and Zhou, You ORCID: https://orcid.org/0000-0002-1743-1291 2016. A deleterious role for Th9/IL-9 in hepatic fibrogenesis. Scientific Reports 6 , 18694. 10.1038/srep18694 |
Abstract
T helper 9 (Th9) cells, a recently recognized Th cell subset, are involved in autoimmune diseases. We aimed to investigate the role of Th9/interleukin-9 (IL-9) in the pathogenesis of hepatic fibrosis. Th9 and Th17 cells were quantified in chronic hepatitis B (CHB) patients with hepatic fibrosis, HBV-associated liver cirrhosis (LC) patients and healthy controls (HC). The percentages of Th9 and Th17 cells, concentrations of IL-9 and IL-17, as well as expression of IL-17, TNF-α, IL-6, IL-4, IL-21, TGF-β1 and IFN-γ were significantly increased in plasma of CHB and LC patients compared with those in HC. Splenic Th9 and Th17 cells, plasma concentrations and liver expression of IL-9 and IL-17A were significantly elevated in mice with hepatic fibrosis compared with controls. Neutralization of IL-9 in mice ameliorated hepatic fibrosis, attenuated the activation of hepatic stellate cells, reduced frequencies of Th9, Th17 and Th1 cells in spleen, and suppressed expression of IL-9, IL-17A, IFN-γ, TGF-β1, IL-6, IL-4 and TNF-α in plasma and liver respectively. Our data suggest a deleterious role of Th9/IL-9 in increasing hepatic fibrosis and exacerbating disease endpoints, indicating that Th9/IL9 based immunotherapy may be a promising approach for treating hepatic fibrosis.
Item Type: | Article |
---|---|
Date Type: | Publication |
Status: | Published |
Schools: | Medicine Systems Immunity Research Institute (SIURI) |
Subjects: | R Medicine > R Medicine (General) |
Publisher: | Nature Publishing Group |
ISSN: | 2045-2322 |
Date of Acceptance: | 23 November 2015 |
Last Modified: | 31 Oct 2022 10:49 |
URI: | https://orca.cardiff.ac.uk/id/eprint/86292 |
Citation Data
Cited 32 times in Scopus. View in Scopus. Powered By Scopus® Data
Actions (repository staff only)
Edit Item |