Publication Name	World Journal of Diabetes
Manuscript ID	41940
Country	United States

Received	2018-09-01 03:23
Peer-Review Started	2018-09-03 01:21
To Make the First Decision	2018-10-17 01:50
Return for Revision	2018-10-17 06:32
Revised	2018-10-23 16:23
Second Decision	2018-11-23 11:05
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2018-11-26 22:14
Articles in Press	2018-11-26 22:14
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2018-12-03 06:18
Publish the Manuscript Online	2018-12-14 01:19

ISSN	1948-9358 (online)
Open Access	This 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 Non Commercial (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/
Copyright	© The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
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Category	Endocrinology & Metabolism
Manuscript Type	Minireviews
Article Title	Unexpected alliance between syndecan-1 and innate-like T cells to protect host from autoimmune effects of interleukin-17
Manuscript Source	Invited Manuscript
All Author List	Anil Kumar Jaiswal, Mohanraj Sadasivam and Abdel Rahim A Hamad
Funding Agency and Grant Number
Corresponding Author	Abdel Rahim A Hamad, PhD, Associate Professor, Department of Pathology, School of Medicine, Johns Hopkins University, Ross 66G, 720 Rutland Ave, Baltimore, MD 21205, United States. ahamad@jhmi.edu
Key Words	Natural killer T cell; Natural killer T 17 cells; Tγδ17 cells; Syndecan-1; Interleukin-17
Core Tip	Core tip: Interleukin-17 (IL-17) is a potent proin­flammatory cytokine that plays a critical role in host defense against fungi and extracellular bacteria. Exce­ssive production of IL-17, however, has been implicated in pathogenesis of many autoimmune diseases. Our recent findings show that natural killer T (NKT) cells and γδ T cells employ syndecan-1 (sdc1), a heparan sulfate proteoglycan that is predominantly expressed by epithelia, to prevent out of control expansion of IL-17-producing subsets of NKT (NKT17) cell and γδ (Tγδ17) cells. In this mini-review, we highlight these findings and briefly discuss their significance for developing new strategies to prevent IL-17-mediated autoimmme diseases.
Publish Date	2018-12-14 01:19
Citation	Jaiswal AK, Sadasivam M, Hamad ARA. Unexpected alliance between syndecan-1 and innate-like T cells to protect host from autoimmune effects of interleukin-17. World J Diabetes 2018; 9(12): 220-225
URL	https://www.wjgnet.com/1948-9358/full/v9/i12/220.htm
DOI	https://dx.doi.org/10.4239/wjd.v9.i12.220

Full Article (PDF)	WJD-9-220.pdf
Full Article (Word)	WJD-9-220.doc
Manuscript File	41940-Review.docx
Answering Reviewers	41940-Answering reviewers.pdf
Audio Core Tip	41940-Audio core tip.mp3
Conflict-of-Interest Disclosure Form	41940-Conflict-of-interest statement.pdf
Copyright License Agreement	41940-Copyright license agreement.pdf
Peer-review Report	41940-Peer-review(s).pdf
Scientific Misconduct Check	41940-Scientific misconduct check.pdf
Scientific Editor Work List	41940-Scientific editor work list.pdf