Abstract
Hepatic macrophages are a remarkably heterogeneous population consisting of self-renewing tissue-resident phagocytes, termed Kupffer cells (KCs), and recruited macrophages derived from peritoneal cavity as well as the bone marrow. KCs are located in the liver sinusoid where they scavenge the microbe from the portal vein to maintain liver homeostasis. Liver injury may trigger hepatic recruitment of peritoneal macrophages and monocyte-derived macrophages. Studies describing macrophage accumulation have shown that hepatic macrophages are involved in the initiation and progression of various liver diseases. They act as tolerogenic antigen-presenting cells to inhibit T-cell activation by producing distinct sets of cytokines, chemokines, and mediators to maintain or resolve inflammation. Furthermore, by releasing regenerative growth factors, matrix metalloproteinase arginase, they promote tissue repair. Recent experiments found that KCs and recruited macrophages may play different roles in the development of liver disease. Given that hepatic macrophages are considerably plastic populations, their phenotypes and functions are likely switching along disease progression. In this review, we summarize current knowledge about the role of tissue-resident macrophages and recruited macrophages in pathogenesis of alcoholic liver disease (ALD), non-alcoholic steatohepatitis (NASH), viral hepatitis, and hepatocellular carcinoma (HCC).
Highlights
Hepatic macrophages, consisting of Kupffer cells (KCs) and recruited macrophages, are the largest population of innate immune cells in the liver
It has been documented that hepatic macrophages accumulate within the portal tracts of alcoholic liver disease (ALD) patients [28], whereas the depletion of hepatic macrophages via the administration of gadolinium chloride (GdCl3) prevents alcohol-induced liver inflammation in the rat [29]. These results suggest that hepatic macrophages play a central role in the pathogenesis of ALD
About 20% of patients who suffer from non-alcoholic fatty liver disease will develop non-alcoholic steatohepatitis (NASH), which is defined by the existence of progressive fibrosis and steatosis with inflammation, leading to hepatocellular carcinoma (HCC) and cirrhosis
Summary
Reviewed by: Xian-Hui He, Jinan University, China Samar H. Specialty section: This article was submitted to Molecular Innate Immunity, a section of the journal
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.