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. 2021 Aug 15;13(8):835–844. doi: 10.4251/wjgo.v13.i8.835

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©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/

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The potential mechanism by which Helicobacter pylori might contribute to autoimmune pancreatitis. H. pylori: Helicobacter pylori; GP: Glycoproteins; Hsp: Heat shock protein; H+/K+ ATPase: H+/K+-adenosine triphosphatase; HLA-DR: Human leukocyte class II DR antigens; CA-II: Carbonic anhydrase type II antigens; ACA-II: Anticarbonic anhydrase II antibody; LF: Lactoferrin; ALF: Antilactoferrin antibody; TLs: T lymphocytes; IFN-ɣ: Interferon-ɣ; anti-Hsps: Antibodies against heat shock proteins; ROMs: Reactive oxygen metabolites.