Søren Egedal Degn

Clinical and immunological parameters of Sjögren's syndrome

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Clinical and immunological parameters of Sjögren's syndrome. / Psianou, Konstantia; Panagoulias, Ioannis; Papanastasiou, Anastasios D et al.

In: Autoimmunity Reviews, Vol. 17, No. 10, 18.10.2018, p. 1053-1064.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperReviewResearchpeer-review

Harvard

Psianou, K, Panagoulias, I, Papanastasiou, AD, de Lastic, A-L, Rodi, M, Spantidea, PI, Degn, SE, Georgiou, P & Mouzaki, A 2018, 'Clinical and immunological parameters of Sjögren's syndrome', Autoimmunity Reviews, vol. 17, no. 10, pp. 1053-1064. https://doi.org/10.1016/j.autrev.2018.05.005

APA

Psianou, K., Panagoulias, I., Papanastasiou, A. D., de Lastic, A-L., Rodi, M., Spantidea, P. I., Degn, S. E., Georgiou, P., & Mouzaki, A. (2018). Clinical and immunological parameters of Sjögren's syndrome. Autoimmunity Reviews, 17(10), 1053-1064. https://doi.org/10.1016/j.autrev.2018.05.005

CBE

Psianou K, Panagoulias I, Papanastasiou AD, de Lastic A-L, Rodi M, Spantidea PI, Degn SE, Georgiou P, Mouzaki A. 2018. Clinical and immunological parameters of Sjögren's syndrome. Autoimmunity Reviews. 17(10):1053-1064. https://doi.org/10.1016/j.autrev.2018.05.005

MLA

Psianou, Konstantia et al. "Clinical and immunological parameters of Sjögren's syndrome". Autoimmunity Reviews. 2018, 17(10). 1053-1064. https://doi.org/10.1016/j.autrev.2018.05.005

Vancouver

Psianou K, Panagoulias I, Papanastasiou AD, de Lastic A-L, Rodi M, Spantidea PI et al. Clinical and immunological parameters of Sjögren's syndrome. Autoimmunity Reviews. 2018 Oct 18;17(10):1053-1064. Epub 2018 Aug 10. doi: 10.1016/j.autrev.2018.05.005

Author

Psianou, Konstantia ; Panagoulias, Ioannis ; Papanastasiou, Anastasios D et al. / Clinical and immunological parameters of Sjögren's syndrome. In: Autoimmunity Reviews. 2018 ; Vol. 17, No. 10. pp. 1053-1064.

Bibtex

@article{816a6f556953483ab6700671f3e1fa3c,
title = "Clinical and immunological parameters of Sj{\"o}gren's syndrome",
abstract = "Sj{\"o}gren's syndrome (SS) is a chronic autoimmune disease that primarily affects the exocrine glands, resulting in their functional impairment. In SS, lymphocytic infiltration of salivary and lacrimal glands, and deposition of several types of autoantibodies, mainly anti-SS-A (anti-Ro) and anti-SS-B (anti-La), lead to chronic inflammation, with xerostomia and keratoconjunctivitis sicca. In its primary form (pSS), SS does not involve additional connective tissue diseases, whereas in its secondary and more common form (sSS), SS presents in association with other rheumatic autoimmune diseases, mainly rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). As in most autoimmune diseases, environmental, hormonal and genetic factors are implicated in SS pathogenesis. In SS T cells predominate in mild lesions, whereas B cells predominate in advanced lesions. Th1, Th2, Th17, follicular helper T (Tfh) cells and regulatory cells (Tregs/Bregs), with their characteristic cytokine profiles, have been implicated in the pathogenesis of SS. It has been suggested that Th1 and Th17 cells initiate SS and, as the disease progresses, Th2 and Tfh cells predominate. It is assumed that, as in all autoimmune and inflammatory conditions, tolerance defects contribute to SS pathogenesis. It is intriguing that in SS it remains unclear which types of regulatory cells are functional and whether they ameliorate or worsen the disease. In this review we present a comprehensive update on SS with emphasis on immune system involvement, and suggest new insights into SS immunopathogenesis.",
author = "Konstantia Psianou and Ioannis Panagoulias and Papanastasiou, {Anastasios D} and {de Lastic}, Anne-Lise and Maria Rodi and Spantidea, {Panagiota I} and Degn, {S{\o}ren E} and Panagiotis Georgiou and Athanasia Mouzaki",
note = "Copyright {\textcopyright} 2018. Published by Elsevier B.V.",
year = "2018",
month = oct,
day = "18",
doi = "10.1016/j.autrev.2018.05.005",
language = "English",
volume = "17",
pages = "1053--1064",
journal = "Autoimmunity Reviews",
issn = "1568-9972",
publisher = "Elsevier Inc.",
number = "10",

}

RIS

TY - JOUR

T1 - Clinical and immunological parameters of Sjögren's syndrome

AU - Psianou, Konstantia

AU - Panagoulias, Ioannis

AU - Papanastasiou, Anastasios D

AU - de Lastic, Anne-Lise

AU - Rodi, Maria

AU - Spantidea, Panagiota I

AU - Degn, Søren E

AU - Georgiou, Panagiotis

AU - Mouzaki, Athanasia

N1 - Copyright © 2018. Published by Elsevier B.V.

PY - 2018/10/18

Y1 - 2018/10/18

N2 - Sjögren's syndrome (SS) is a chronic autoimmune disease that primarily affects the exocrine glands, resulting in their functional impairment. In SS, lymphocytic infiltration of salivary and lacrimal glands, and deposition of several types of autoantibodies, mainly anti-SS-A (anti-Ro) and anti-SS-B (anti-La), lead to chronic inflammation, with xerostomia and keratoconjunctivitis sicca. In its primary form (pSS), SS does not involve additional connective tissue diseases, whereas in its secondary and more common form (sSS), SS presents in association with other rheumatic autoimmune diseases, mainly rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). As in most autoimmune diseases, environmental, hormonal and genetic factors are implicated in SS pathogenesis. In SS T cells predominate in mild lesions, whereas B cells predominate in advanced lesions. Th1, Th2, Th17, follicular helper T (Tfh) cells and regulatory cells (Tregs/Bregs), with their characteristic cytokine profiles, have been implicated in the pathogenesis of SS. It has been suggested that Th1 and Th17 cells initiate SS and, as the disease progresses, Th2 and Tfh cells predominate. It is assumed that, as in all autoimmune and inflammatory conditions, tolerance defects contribute to SS pathogenesis. It is intriguing that in SS it remains unclear which types of regulatory cells are functional and whether they ameliorate or worsen the disease. In this review we present a comprehensive update on SS with emphasis on immune system involvement, and suggest new insights into SS immunopathogenesis.

AB - Sjögren's syndrome (SS) is a chronic autoimmune disease that primarily affects the exocrine glands, resulting in their functional impairment. In SS, lymphocytic infiltration of salivary and lacrimal glands, and deposition of several types of autoantibodies, mainly anti-SS-A (anti-Ro) and anti-SS-B (anti-La), lead to chronic inflammation, with xerostomia and keratoconjunctivitis sicca. In its primary form (pSS), SS does not involve additional connective tissue diseases, whereas in its secondary and more common form (sSS), SS presents in association with other rheumatic autoimmune diseases, mainly rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). As in most autoimmune diseases, environmental, hormonal and genetic factors are implicated in SS pathogenesis. In SS T cells predominate in mild lesions, whereas B cells predominate in advanced lesions. Th1, Th2, Th17, follicular helper T (Tfh) cells and regulatory cells (Tregs/Bregs), with their characteristic cytokine profiles, have been implicated in the pathogenesis of SS. It has been suggested that Th1 and Th17 cells initiate SS and, as the disease progresses, Th2 and Tfh cells predominate. It is assumed that, as in all autoimmune and inflammatory conditions, tolerance defects contribute to SS pathogenesis. It is intriguing that in SS it remains unclear which types of regulatory cells are functional and whether they ameliorate or worsen the disease. In this review we present a comprehensive update on SS with emphasis on immune system involvement, and suggest new insights into SS immunopathogenesis.

U2 - 10.1016/j.autrev.2018.05.005

DO - 10.1016/j.autrev.2018.05.005

M3 - Review

C2 - 30103041

VL - 17

SP - 1053

EP - 1064

JO - Autoimmunity Reviews

JF - Autoimmunity Reviews

SN - 1568-9972

IS - 10

ER -