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. 2021 Sep 23;12:729143. doi: 10.3389/fimmu.2021.729143

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Copyright © 2021 Patel, Liu, Davies, Brown, Kelly, Scheel-Toellner, Reynolds and Stamataki

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Alcohol related liver disease pathogenesis. Excessive alcohol consumption (1) induces inflammation and results in increased gut permeability (2), allowing bacterial translocation of LPS. Inflammatory mediators damage hepatocytes, resulting in the release of cellular debris (3). Self-antigens are engulfed by antigen presenting cells (4) and presented to autoreactive T cells (5), which stimulate autoreactive B cells (6). Activated B cells then migrate to secondary lymphoid tissues and undergo germinal centre reactions (7) where B cells with increased affinity receptors differentiate into memory B cells and PCs (8). The secretion of inflammatory mediators and autoantibodies from memory B cells and PCs further damage hepatocytes (9). The formation of immune complexes induces further inflammation (10). These immune complexes are engulfed by APCs. Created with BioRender.com.