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IL-33-ST2 Axis in Liver Disease: Progression and Challenge.
Sun, Zijian; Chang, Binxia; Gao, Miaomiao; Zhang, Jiyuan; Zou, Zhengsheng.
Afiliação
  • Sun Z; Center of Non-Infectious Liver Diseases, Peking University 302 Clinical Medical School, Beijing, China.
  • Chang B; Center of Non-Infectious Liver Diseases, Beijing 302 Hospital, Beijing, China.
  • Gao M; Center of Non-Infectious Liver Diseases, Peking University 302 Clinical Medical School, Beijing, China.
  • Zhang J; Treatment and Research Center for Infectious Diseases, Beijing 302 Hospital, Beijing, China.
  • Zou Z; Center of Non-Infectious Liver Diseases, Peking University 302 Clinical Medical School, Beijing, China.
Mediators Inflamm ; 2017: 5314213, 2017.
Article em En | MEDLINE | ID: mdl-29180837
ABSTRACT
The new member of the IL-1 family, interleukin-33 (IL-33), participates in the progression of a variety of diseases through binding with its receptor ST2. Recently, much clinical evidence and experimental data have indicated that IL-33 is associated with various liver diseases. This review primarily addresses the relationship between IL-33 and several hepatic diseases. IL-33 can alleviate high-fat diet- (HFD-) induced hepatic steatosis and insulin resistance, and IL-33 acts as an alarmin, which quickly triggers the immune system to respond to virus invasion and toxic damage to the liver. However, when liver injury is chronic, IL-33 promotes Th2 reactions and hepatic stellate cell (HSC) activity, facilitating progression to liver fibrosis. The complicated functions of IL-33 should be considered before its clinical application.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Interleucina-33 / Hepatopatias Limite: Humans Idioma: En Revista: Mediators Inflamm Assunto da revista: BIOQUIMICA / PATOLOGIA Ano de publicação: 2017 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Interleucina-33 / Hepatopatias Limite: Humans Idioma: En Revista: Mediators Inflamm Assunto da revista: BIOQUIMICA / PATOLOGIA Ano de publicação: 2017 Tipo de documento: Article País de afiliação: China