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New insights into an old paradigm: why IgA accumulates in alcoholic liver disease and what could be its role
  1. Dragos Ciocan1,
  2. Williams Turpin2
  1. 1 Systems Immunology Department, Weizmann Institute of Science, Rehovot, Israel
  2. 2 Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, Toronto, Ontario, Canada
  1. Correspondence to Dr Williams Turpin, Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, Toronto, Ontario, Canada; williams.turpin{at}utoronto.ca

http://dx.doi.org/10.1136/gutjnl-2022-329415

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    Alcoholic liver disease (ALD) is the most prevalent cause of chronic liver disease in western countries with highly morbid complications, such as alcohol-associated hepatitis and limited therapeutic options.1 The pathogenesis of ALD is highly influenced by the gut-liver axis1 and some of the key features of ALD include dysbiosis (bacterial, fungal and viral), increased intestinal permeability and translocation of bacterial ligands that activate inflammatory pathways in the liver (figure 1). In this context, the defence mechanism especially at the intestinal level are essential for the control of bacterial translocation. Among these mechanisms, secretory immunoglobulins are essential for the protection of the mucosal surface by binding and neutralising harmful pathogens. However, patients with ALD have increased systemic IgA levels2 and IgA deposits in hepatic sinusoids. While these observations were made decades ago, their cause and role in ALD pathogenesis remained unknown.

    Figure 1

    Red indicates mechanisms involved in alcoholic liver disease pathogenesis. Blue indicates an unknown mechanism involved in regulation of pIgR. Green indicates potential therapeutic tool to modulate disease severity or onset. pIgR, polymeric immunoglobulin receptor. Created with BioRender.com.

    In this context, we read with great interest the article by Hendrikx et al 3 who deeply characterised the function of polymeric immunoglobulin …

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    Footnotes

    • DC and WT contributed equally.

    • Contributors DC and WT contributed equaly.

    • Funding DC is a recipient of European Union’s Horizon 2020 research and innovation programme under Marie Sklodowska‐Curie grant agreement no. 101068605.

    • Competing interests None declared.

    • Provenance and peer review Commissioned; internally peer reviewed.

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