The Emerging Role of B Cells in the Pathogenesis of NAFLD.
The Emerging Role of B Cells in the Pathogenesis of NAFLD.
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DOI：
10.1002/hep.31889
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发表时间：
2021-10
期刊：
影响因子：
--
通讯作者：
Revelo XS
中科院分区：
文献类型：
--
作者：
Barrow F;Khan S;Wang H;Revelo XS
非酒精性脂肪肝是世界范围内肝功能异常的主要原因之一。NAFLD是指从非酒精性脂肪肝到NASH的一组肝脏疾病，涉及炎症、肝细胞损伤和纤维化。NASH炎症的触发是疾病发展过程中的一个关键事件，需要确定启动或失调这一过程的因素，以制定预防或治疗策略。B细胞与几种自身免疫性和炎症性疾病有关。然而，它们在NAFLD和NASH发病机制中的作用还不是很清楚。该综述讨论了肝内B细胞参与NAFLD进展的新证据。我们强调了NAFLD过程中B细胞激活的潜在机制，如肝脏B细胞激活因子的表达增加，氧化应激增强，以及肠道微生物产物的移位。我们讨论了B细胞促进NAFLD的可能效应功能，包括促炎细胞因子的产生和肝内T细胞和巨噬细胞的调节。最后，我们强调了调节性细胞和IgA+B细胞在NASH相关肝细胞癌发病机制中的作用。在这篇综述中，我们认为需要进一步的研究来研究B细胞靶向策略治疗NAFLD的潜力。
NAFLD is one of the leading causes of abnormal liver function worldwide. NAFLD refers to a group of liver conditions ranging from nonalcoholic fatty liver to NASH, which involves inflammation, hepatocellular damage, and fibrosis. Triggering of inflammation in NASH is a key event in the progression of the disease, and identifying the factors that initiate or dysregulate this process is needed to develop strategies for its prevention or treatment. B cells have been implicated in several autoimmune and inflammatory diseases. However, their role in the pathogenesis of NAFLD and NASH is less clear. This review discusses the emerging evidence implicating intrahepatic B cells in the progression of NAFLD. We highlight the potential mechanisms of B‐cell activation during NAFLD, such as increased hepatic expression of B‐cell–activating factor, augmented oxidative stress, and translocation of gut‐derived microbial products. We discuss the possible effector functions by which B cells promote NAFLD, including the production of proinflammatory cytokines and regulation of intrahepatic T cells and macrophages. Finally, we highlight the role of regulatory and IgA+ B cells in the pathogenesis of NASH‐associated HCC. In this review, we make the case that future research is needed to investigate the potential of B‐cell–targeting strategies for the treatment of NAFLD.
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影响因子：
13.5
作者：
Harley, Isaac T. W.;Stankiewicz, Traci E.;Giles, Daniel A.;Softic, Samir;Flick, Leah M.;Cappelletti, Monica;Sheridan, Rachel;Xanthakos, Stavra A.;Steinbrecher, Kris A.;Sartor, R. Balfour;Kohli, Rohit;Karp, Christopher L.;Divanovic, Senad
通讯作者：
Divanovic, Senad
DOI：
10.1002/art.39856
发表时间：
2017-02
期刊：
Arthritis & rheumatology (Hoboken, N.J.)
影响因子：
--
作者：
Clowse ME;Wallace DJ;Furie RA;Petri MA;Pike MC;Leszczyński P;Neuwelt CM;Hobbs K;Keiserman M;Duca L;Kalunian KC;Galateanu C;Bongardt S;Stach C;Beaudot C;Kilgallen B;Gordon C;EMBODY Investigator Group
通讯作者：
EMBODY Investigator Group
影响因子：
17.1
作者：
Balmer, Maria L.;Slack, Emma;Macpherson, Andrew J.
通讯作者：
Macpherson, Andrew J.
影响因子：
64.8
作者：
Dudek, Michael;Pfister, Dominik;Knolle, Percy A.
通讯作者：
Knolle, Percy A.
影响因子：
25.7
作者：
Heier, Eva-Carina;Meier, Anna;Lukacs-Kornek, Veronika
通讯作者：
Lukacs-Kornek, Veronika