ID 57791
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Gion, Yuka Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Takeuchi, Mai Department of Pathology, Kurume University School of Medicine
Shibata, Rei Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Takata, Katsuyoshi Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kakenhi
Miyata-Takata, Tomoko Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Orita, Yorihisa Department of Otolaryngology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kakenhi
Tachibana, Tomoyasu Department of Otolaryngology, Himeji Red Cross Hospital
Yoshino, Tadashi Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kakenhi
Sato, Yasuharu Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kakenhi
Abstract
Immunoglobulin (Ig) G4-related disease (IgG4-RD) is a systemic disorder involving benign mass formation due to fibrosis and intense lymphoplasmacytosis; the chronic inflammation associated with the disease might also contribute to oncogenesis. Activation-induced cytidine deaminase (AID), normally expressed in germinal centre activated B-cells, is an enzyme that edits DNA/RNA and induces somatic hypermutation and Ig class switching. AID expression is strictly controlled under physiological conditions; however, chronic inflammation and some infectious agents induce its up-regulation. AID is overexpressed in various cancers and may be important in chronic inflammation-associated oncogenesis. We examined AID expression in IgG4-related sialadenitis (n = 14), sialolithiasis (nonspecific inflammation, n = 13), and normal submandibular glands (n = 13) using immunohistochemistry and quantitative real-time polymerase chain reaction (qPCR). Immunohistochemistry revealed significantly more AID-expressing cells in IgG4-related sialadenitis than in sialolithiasis or normal submandibular gland samples (P = 0.02 and P < 0.01, respectively); qPCR yielded similar results. Thus, AID was significantly more up-regulated and had higher expression in extra-germinal centres in IgG4-RD than in non-specific inflammation or normal conditions. This report suggests that IgG4-RD has several specific causes of AID up-regulation in addition to inflammation. Furthermore, chronic inflammation-associated AID-mediated oncogenesis is possible in IgG4-RD.
Published Date
2019-1-24
Publication Title
Scientific Reports
Volume
volume9
Publisher
Nature Publishing Group
Start Page
761
ISSN
2045-2322
Content Type
Journal Article
language
英語
OAI-PMH Set
岡山大学
Copyright Holders
© The Author(s) 2019
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DOI
Web of Science KeyUT
Related Url
isVersionOf https://doi.org/10.1038/s41598-018-37404-x
License
https://creativecommons.org/licenses/by/4.0/
Funder Name
Japan Society for the Promotion of Science
助成番号
JP16K08666
17K17894