Publication Name	World Journal of Immunology
Manuscript ID	21245
Country	Mexico

Received	2015-07-02 08:51
Peer-Review Started	2015-07-08 12:05
To Make the First Decision	2015-09-16 13:53
Return for Revision	2015-09-18 17:35
Revised	2015-09-22 23:08
Second Decision	2015-11-02 14:34
Accepted by Journal Editor-in-Chief	2015-11-02 16:07
Accepted by Executive Editor-in-Chief	2015-11-17 09:22
Articles in Press	2015-11-17 09:22
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2015-11-18 09:42
Publish the Manuscript Online	2015-11-27 16:41

ISSN	2219-2824 (online)
Open Access	This article is an open-access article which 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) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
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Category	Rheumatology
Manuscript Type	Minireviews
Article Title	Lessons from Sjögren’s syndrome etiopathogenesis: Novel cellular and molecular targets
Manuscript Source	Invited Manuscript
All Author List	José C Crispín, Florencia Rosetti and Gabriela Hernández-Molina
Funding Agency and Grant Number	Funding Agency Grant Number El Consejo Nacional de Ciencia y Tecnología (CONACyT) INFR-2015-253812
Corresponding Author	Gabriela Hernández-Molina, MD, Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Vasco de Quiroga #15, Mexico City 14080, Mexico. gabyhm@yahoo.com
Key Words	Sjögren’s syndrome; Pathogenesis; Therapy; T cell; Cytokines
Core Tip	Sjogren’s syndrome (SS) is a complex entity caused by an autoimmune process that encompasses both an anti-acinar and a systemic response. Exocrine gland infiltration is probably primarily responsible for the destruction of the acinar cells and consequently for the development of sicca symptoms. The participation of diverse chemokines, activated T cells and B cells, cytokines and cytokine signaling pathways has been recognized. The aim of this review is to discuss some aspects of SS pathogenesis and emphasize the potential opportunities where therapeutic interventions might be useful.
Publish Date	2015-11-27 16:41
Citation	Crispín JC, Rosetti F, Hernández-Molina G. Lessons from Sjögren’s syndrome etiopathogenesis: Novel cellular and molecular targets. World J Immunol 2015; 5(3): 152-159
URL	http://www.wjgnet.com/2219-2824/full/v5/i3/152.htm
DOI	http://dx.doi.org/10.5411/wji.v5.i3.152

Full Article (PDF)	WJI-5-152.pdf
Full Article (Word)	WJI-5-152.doc
Manuscript File	21245-Review.doc
Answering Reviewers	21245-Answering reviewers.pdf
Audio Core Tip	21245-Audio core tip.mp3
Conflict-of-Interest Disclosure Form	21245-Conflict-of-interest statement.pdf
Copyright License Agreement	21245-Copyright assignment.pdf
Supplementary Material	Supplementary_Material_20150702021534.pdf
Peer-review Report	21245-Peer-review(s).pdf
Journal Editor-in-Chief Review Report	21245-Journal editor-in-chief review report.pdf
Scientific Misconduct Check	21245-Scientific misconduct check.pdf
Scientific Editor Work List	21245-Scientific editor work list.pdf