Publication Name	World Journal of Gastroenterology
Manuscript ID	74878
Country	Japan

Received	2022-01-10 05:19
Peer-Review Started	2022-01-10 05:21
To Make the First Decision
Return for Revision	2022-04-16 07:04
Revised	2022-04-21 08:46
Second Decision	2022-06-15 02:59
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief	2022-06-16 17:17
Articles in Press	2022-06-16 17:17
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2022-06-22 07:07
Publish the Manuscript Online	2022-07-13 07:30

ISSN	1007-9327 (print) and 2219-2840 (online)
Open Access	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: https://creativecommons.org/Licenses/by-nc/4.0/
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Category	Immunology
Manuscript Type	Minireviews
Article Title	Alterations of autophagic and innate immune responses by the Crohn’s disease-associated ATG16L1 mutation
Manuscript Source	Invited Manuscript
All Author List	Natsuki Okai, Tomohiro Watanabe, Kosuke Minaga, Ken Kamata, Hajime Honjo and Masatoshi Kudo
ORCID	Author(s) ORCID Number Natsuki Okai http://orcid.org/0000-0002-3167-4927 Tomohiro Watanabe http://orcid.org/0000-0001-7781-6305 Kosuke Minaga http://orcid.org/0000-0001-5407-7925 Ken Kamata http://orcid.org/0000-0003-1568-0769 Hajime Honjo http://orcid.org/0000-0002-0888-3384 Masatoshi Kudo http://orcid.org/0000-0002-4102-3474
Funding Agency and Grant Number
Corresponding Author	Tomohiro Watanabe, MD, PhD, Associate Professor, Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama 589-8511, Osaka, Japan. tomohiro@med.kindai.ac.jp
Key Words	ATG16L1; Crohn’s disease; Autophagy; Innate immunity; Cytokine; Pattern recognition receptors
Core Tip	The loss-of-function mutation T300A in autophagy related 16 like 1 (ATG16L1) increases the risk of Crohn’s disease (CD). ATG16L1 is a multifunctional protein involved in autophagy and innate immunity. The CD-associated ATG16L1 mutation T300A leads to overgrowth of intestinal microbiota and enhanced pro-inflammatory cytokine responses, which disrupt intestinal immune homeostasis. In this minireview article, we have summarized the immunopathogenesis of CD in the presence of ATG16L1 mutation.
Publish Date	2022-07-13 07:30
Citation	Okai N, Watanabe T, Minaga K, Kamata K, Honjo H, Kudo M. Alterations of autophagic and innate immune responses by the Crohn’s disease-associated ATG16L1 mutation. World J Gastroenterol 2022; 28(26): 3063-3070
URL	https://www.wjgnet.com/1007-9327/full/v28/i26/3063.htm
DOI	https://dx.doi.org/10.3748/wjg.v28.i26.3063

Full Article (PDF)	WJG-28-3063.pdf
Full Article (Word)	WJG-28-3063.docx
Manuscript File	74878_Auto_Edited_LM.docx
Answering Reviewers	74878-Answering reviewers.pdf
Audio Core Tip	74878-Audio core tip.m4a
Conflict-of-Interest Disclosure Form	74878-Conflict-of-interest statement.pdf
Copyright License Agreement	74878-Copyright license agreement.pdf
Non-Native Speakers of English Editing Certificate	74878-Language certificate.pdf
Peer-review Report	74878-Peer-review(s).pdf
Scientific Editor Work List	74878-Scientific editor work list.pdf