<small lang="MxMnMqr"></small> <b dropzone="em9zo"></b> Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The . gov means it’s official. Federal government websites often end in . gov or . mil. Before sharing sensitive information, make sure you’re on a federal government site. VSports app下载.

Https

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. V体育官网.

. 2016 Jul 11;30(1):161-175.
doi: 10.1016/j.ccell.2016.05.020.

Metabolic Inflammation-Associated IL-17A Causes Non-alcoholic Steatohepatitis and Hepatocellular Carcinoma (V体育官网入口)

Ana L Gomes  1 , Ana Teijeiro  1 , Stefan Burén  1 , Krishna S Tummala  1 , Mahmut Yilmaz  1 , Ari Waisman  2 , Jean-Philippe Theurillat  3 , Cristian Perna  4 , Nabil Djouder  5
Affiliations
Free article

Metabolic Inflammation-Associated IL-17A Causes Non-alcoholic Steatohepatitis and Hepatocellular Carcinoma (V体育平台登录)

Ana L Gomes et al. Cancer Cell. .
Free article

"VSports注册入口" Abstract

Obesity increases hepatocellular carcinoma (HCC) risks via unknown mediators. We report that hepatic unconventional prefoldin RPB5 interactor (URI) couples nutrient surpluses to inflammation and non-alcoholic steatohepatitis (NASH), a common cause of HCC. URI-induced DNA damage in hepatocytes triggers inflammation via T helper 17 (Th17) lymphocytes and interleukin 17A (IL-17A). This induces white adipose tissue neutrophil infiltration mediating insulin resistance (IR) and fatty acid release, stored in liver as triglycerides, causing NASH. NASH and subsequently HCC are prevented by pharmacological suppression of Th17 cell differentiation, IL-17A blocking antibodies, and genetic ablation of the IL-17A receptor in myeloid cells. Human hepatitis, fatty liver, and viral hepatitis-associated HCC exhibit increased IL-17A correlating positively with steatosis VSports手机版. IL-17A blockers may prevent IR, NASH, and HCC in high-risk patients. .

PubMed Disclaimer

Comment in (V体育安卓版)

Publication types

MeSH terms

V体育安卓版 - Substances

LinkOut - more resources (V体育官网入口)