Copyright
©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Immunol. Nov 27, 2015; 5(3): 152-159
Published online Nov 27, 2015. doi: 10.5411/wji.v5.i3.152
Published online Nov 27, 2015. doi: 10.5411/wji.v5.i3.152
Lessons from Sjögren’s syndrome etiopathogenesis: Novel cellular and molecular targets
José C Crispín, Florencia Rosetti, Gabriela Hernández-Molina, Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City 14080, Mexico
Author contributions: All the authors wrote the manuscript.
Supported by Grant INFR-2015-253812 from El Consejo Nacional de Ciencia y Tecnología (CONACyT).
Conflict-of-interest statement: The authors have no conflict of interest to declare.
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/
Correspondence to: 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
Telephone: +52-55-54850766 Fax: +52-55-55732096
Received: July 2, 2015
Peer-review started: July 8, 2015
First decision: September 18, 2015
Revised: September 22, 2015
Accepted: November 13, 2015
Article in press: November 17, 2015
Published online: November 27, 2015
Peer-review started: July 8, 2015
First decision: September 18, 2015
Revised: September 22, 2015
Accepted: November 13, 2015
Article in press: November 17, 2015
Published online: November 27, 2015
Core Tip
Core tip: Sjögren’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.