Sjögren’s Syndrome—Study of Autoantigens and Autoantibodies

Routsias, John G.; Tzioufas, Athanasios G.

doi:10.1007/s12016-007-8003-8

Cited by 110 publications

(85 citation statements)

References 151 publications

(132 reference statements)

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“…These Abs are detected in serum and can be produced locally in the affected salivary glands (39). Anti-SSB/La Abs are accompanied by anti-SSA/Ro Abs, whereas anti-SSA/Ro Abs can be found either with or without anti-SSB/La Abs (40). In this study, serum titers of anti-SSA/Ro and anti-SSB/La Abs were evaluated relative to Zp and CYP1A1 promoter activities.…”

Section: The Relationship Between Ahr Activation and Autoantibodies Imentioning

confidence: 99%

Aryl Hydrocarbon Receptor-Mediated Induction of EBV Reactivation as a Risk Factor for Sjögren’s Syndrome

Inoue

Mishima

Yamamoto-Yoshida

et al. 2012

The Journal of Immunology

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The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that mediates a variety of biological effects by binding to environmental pollutants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin). Although numerous animal studies have demonstrated the harmful effects of dioxins, it remains controversial whether dioxins pose a risk to human health. Enhanced lytic replication of EBV is a risk factor for the development of autoimmune diseases and cancers. This study evaluated the possibility that ligand-activated AhR reactivates EBV. EBV reactivation and AhR transactivation were evaluated with luciferase assays. Saliva samples were collected from 19 patients with primary Sjögren’s syndrome (SS). Control saliva samples were obtained from 10 healthy individuals and nine patients with severe dry mouth. TCDD enhanced BZLF1 transcription, which mediates the switch from the latent to the lytic form of EBV infection in EBV-positive B cell lines and in a salivary gland epithelial cell line. Moreover, TCDD-induced increases in BZLF1 mRNA and EBV genomic DNA levels were confirmed in the B cell lines. Saliva from SS patients activated the transcription of both CYP1A1 and BZLF1. Additionally, there was a positive correlation between CYP1A1 and BZLF1 promoter activities. AhR ligands elicited the reactivation of EBV in activated B cells and salivary epithelial cells, and these ligands are involved in SS. Our findings reveal novel aspects of the biological effects of dioxin and the AhR-dependent pathogenesis of autoimmune diseases.

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Section: The Relationship Between Ahr Activation and Autoantibodies Imentioning

confidence: 99%

Aryl Hydrocarbon Receptor-Mediated Induction of EBV Reactivation as a Risk Factor for Sjögren’s Syndrome

Inoue

Mishima

Yamamoto-Yoshida

et al. 2012

The Journal of Immunology

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“…This is the case since anti-M 3 mAChR IgG binds to, and activates, the mAChR subtype M 3 of the salivary gland. This produces xerostomia and glandular parasympathetic dysfunction, which in the chronic course of the disease, results also in severe extraglandular manifestations [9] [10] [11].…”

Section: Discussionmentioning

confidence: 99%

“…It is known that anti-Ro/SSA and anti-La/SSB antibodies are directed against ribonucleoprotein complexes [11]. Their localization is mainly cytoplasmic [12] and the increased expression of Ro52 in SS and SLE patients is probably implicated positively or negatively in the alteration of cellular immune responses and in the increased apoptosis observed in pSS patients [13] [14].…”

mentioning

confidence: 99%

Role of M<sub>3</sub> Muscarinic Acethylcholine Receptor Antibodies as a New Marker in Primary Sjögren Syndrome

Reina¹,

Pisoni²,

Arana³

et al. 2017

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Aims: This paper investigates the presence of M 3 muscarinic acetylcholine receptor autoantibody present in the serum of patients with primary Sjögren syndrome (pSS). Main methods: We detected the levels of M 3 mAChR peptide IgG, PGE 2 , IL-1β in serum of SS patients using the enzyme-linked immune sorbent assay (ELISA). To measure the quantity of nitrite/nitrate, we used Griess reagent system. Key findings: Titres of M 3 mAChR antibody in sera from SS patients are significantly enhanced compared to healthy subjects (control). The enhancement of these autoantibodies is accompanied by the increase of the levels of PGE 2 , IL-1β and nitrite/nitrate in serum. Under in vitro conditions, the synthetic human M 3 peptide impaires the increment of M 3 mAChR antibody but not that of nati-Ro/SSA antibody. In positive anti-Ro/SSA antibody patients, the increment of M 3 mAChR peptide IgG and the measured pro-inflammatory substances is related. Significance: On this basis, anti M 3 mAChR peptide IgG can be said to act as a modulator of the immune system and to play a role in the host-chronic increment of proinflammatory substances in SS patients with positive Ro/SSA antibody. This association between the antibody and the pathogenesis of SS disease may result in useful predicting SS.

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“…[16][17][18] The presence of autoantibodies Ro/SSA and La/SSB was found to be generally associated with a longer disease duration, increased frequency of nonexocrine manifestations and a higher intensity of lymphocytic infi ltrates invading the minor salivary glands. 19 Recent case reports and some research have shown that autoantibodies against α-fodrin may be used in the diagnosis and may also be considered as an activation marker of SS with dry eye.…”

Section: Lacrimal Gland Infl Ammationmentioning

confidence: 99%

The role of inflammation and antiinflammation therapies in keratoconjunctivitis sicca

Gümüş

Cavanagh

2008

OPTH

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Purpose: To review and integrate recent advances in identifying the role of infl ammation in the pathogenesis of dry eye conditions and the biological rationale and practical clinical aspects of newer, antiinfl ammatory theories. Methods: A comprehensive literature survey. Results and conclusion: Keratoconjunctivitis Sicca (KCS) is a multifactorial and complex disorder in which ocular surface infl ammations play a central role. Identifi cation of specifi c CD4-T-Cell pathways and the recent recognition of targeting of alpha-fodrin suggest a case for novel new therapeutic aspects such as anti-CD4 monoclonal antibodies, systemic linoleic and gamma-linolenic acids, and omega-6 essential fatty acids. Replacement of tear volume with nonpreserved wetting agents and standard typical antiinfl ammatory corticosteroid and/or cyclosporine A continues to be central current conventional therapy for KCS. Keywords: dry eye, keratoconjunctivitis sicca, antiinfl ammatory therapy Dry eye disease or keratoconjunctivitis sicca (KCS) is a common disorder which refers to a spectrum of ocular surface diseases with multiple etiologies.1 KCS is associated with symptoms of ocular discomfort such as burning, sense of dryness, foreign body sensation, ocular pain, and is sometimes associated with photophobia, blurred vision, visual fatigue, and sight-threatening corneal complications in severe cases. 2,3Epidemiologic studies have stated that more than 6% of the population complains of dry eye symptoms, and this ratio increases to 15% over the age of 65. [4][5][6] Most of the studies have also found an increasing prevalence with aging and greater prevalence among women due to the hormonal status. 4,6,7 Pathogenesis of KCS has not been completely clarified. Even though KCS has been thought of classically and basically as a condition of tear deficiency, whether caused by decreased lacrimation or excessive evaporation, it is a complex disorder. Many clinicopathological entities involving tear film, lacrimal glands, eyelids, and a wide spectrum of ocular surface cells, including epithelial, inflammatory, immune, and goblet cells may play a role in its pathogenesis. 2,8Over the past years, as a result of numerous studies, new concepts of pathogenesis have shown that KCS seems to be caused by infl ammation mediated by T-cell lymphocytes. [9][10][11] This fi nding has also been augmented by the studies investigating the role of antiinfl ammatory therapies. For instance, the treatment of KCS gained a new dimension with the approval of topical 0.05% cyclosporine A (Restasis) (Allergan, Inc., package insert for Restasis) by the US Food and Drug Administration. Consequently, because of the increasing importance of the role of infl ammation and the use of cyclosporine eye drops, the goal of this review article is to provide the readers with an overview of Clinical Ophthalmology downloaded from https://www.dovepress.com/ by 35.167.132.9 on 10-May-2018 For personal use only.Powered by TCPDF (www.tcpdf.org)

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Sjögren’s Syndrome—Study of Autoantigens and Autoantibodies

Cited by 110 publications

References 151 publications

Aryl Hydrocarbon Receptor-Mediated Induction of EBV Reactivation as a Risk Factor for Sjögren’s Syndrome

Aryl Hydrocarbon Receptor-Mediated Induction of EBV Reactivation as a Risk Factor for Sjögren’s Syndrome

Role of M<sub>3</sub> Muscarinic Acethylcholine Receptor Antibodies as a New Marker in Primary Sjögren Syndrome

The role of inflammation and antiinflammation therapies in keratoconjunctivitis sicca

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Sjögren’s Syndrome—Study of Autoantigens and Autoantibodies

Cited by 110 publications

References 151 publications

Aryl Hydrocarbon Receptor-Mediated Induction of EBV Reactivation as a Risk Factor for Sjögren’s Syndrome

Aryl Hydrocarbon Receptor-Mediated Induction of EBV Reactivation as a Risk Factor for Sjögren’s Syndrome

Role of M&lt;sub&gt;3&lt;/sub&gt; Muscarinic Acethylcholine Receptor Antibodies as a New Marker in Primary Sj&#246;gren Syndrome

The role of inflammation and antiinflammation therapies in keratoconjunctivitis sicca

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Role of M<sub>3</sub> Muscarinic Acethylcholine Receptor Antibodies as a New Marker in Primary Sjögren Syndrome