B cell dysregulation in primary Sjögren’s syndrome: A review

Ibrahem, Hazim Mahmoud

doi:10.1016/j.jdsr.2019.09.006

Cited by 49 publications

(28 citation statements)

References 90 publications

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“…Two chemokines involved in the attraction of T-cells in SS SG are CXCL9 and CXCL10 [ 123 ]. In SS SG, T cells are likely to be involved in the disruption of the glandular architecture throughout the apoptosis mechanism mediated by FasL pathway [ 124 ], by a direct cytotoxic activity involving the release of perforin and/or secretion of cytokines and by the activation of B cells [ 125 ]. Th17 cells represent another subpopulation of T-cells strongly activated in SS patients [ 126 ].…”

Section: Physiopathology Of Sjögren’s Syndromementioning

confidence: 99%

Current State of Knowledge on Primary Sjögren’s Syndrome, an Autoimmune Exocrinopathy

Parisis

Chivasso

Perret

et al. 2020

JCM

112

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Primary Sjögren’s syndrome (pSS) is a chronic systemic autoimmune rheumatic disease characterized by lymphoplasmacytic infiltration of the salivary and lacrimal glands, whereby sicca syndrome and/or systemic manifestations are the clinical hallmarks, associated with a particular autoantibody profile. pSS is the most frequent connective tissue disease after rheumatoid arthritis, affecting 0.3–3% of the population. Women are more prone to develop pSS than men, with a sex ratio of 9:1. Considered in the past as innocent collateral passive victims of autoimmunity, the epithelial cells of the salivary glands are now known to play an active role in the pathogenesis of the disease. The aetiology of the “autoimmune epithelitis” still remains unknown, but certainly involves genetic, environmental and hormonal factors. Later during the disease evolution, the subsequent chronic activation of B cells can lead to the development of systemic manifestations or non-Hodgkin’s lymphoma. The aim of the present comprehensive review is to provide the current state of knowledge on pSS. The review addresses the clinical manifestations and complications of the disease, the diagnostic workup, the pathogenic mechanisms and the therapeutic approaches.

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Section: Physiopathology Of Sjögren’s Syndromementioning

confidence: 99%

Current State of Knowledge on Primary Sjögren’s Syndrome, an Autoimmune Exocrinopathy

Parisis

Chivasso

Perret

et al. 2020

JCM

112

View full text Add to dashboard Cite

show abstract

“…It was previously concluded that B cell dysregulation occur in the pSS with the decrease in the percentage of CD27+ memory B cells in peripheral blood and an increase in the CD27+ memory B cells in the affected glands (31). B lymphocytes, by their nature, generally exhibit increased activation states in pSS.…”

Section: Discussionmentioning

confidence: 99%

1,25-dihydroxyvitamin D3 regulates t helper and b lymphocyte responses substantially in drug-naive primary Sjögren’s syndrome patients’ mononuclear cells

et al. 2021

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Objectives: A correlation between vitamin D deficiency and primary Sjögren's Syndrome (pSS) has already been described. The limited data have been reported regarding the pathological relevance of vitamin D in primary Sjögren's syndrome. In this study, the peripheral blood mononuclear cells were cocultured with 1,25-dihydroxyvitaminD3 to determine the modulatory effect of vitamin D3 on T and B lymphocyte phenotypes in pSS.Method: Venous blood samples were collected from 11 in treatment phase and 9 drug-naive pSS patients. Peripheral blood mononuclear cells (PBMC) were isolated and separately cultured in the presence and absence of 1,25-dihydroxyvitaminD3 (10mM) for 5 days of culture period. Lymphocyte proliferation was analyzed for CFSE signaling via flow cytometry. CD3+CD4+ cells were analyzed for intracellular IFN- and IL-17 expressions. CD19+IgD cells were analyzed for CD38 and CD27 expressions to evaluate naïve and memory B cell subsets. Culture supernatants were analyzed for the IFN-, IL-17 and IL-10 cytokine secretions via flow cytometry.Results: 1,25-dihydroxyvitaminD3 significantly decreased Th lymphocyte proliferative responses in drug-naïve (p<0.005) and treated pSS patients (p<0.05), and B lymphocyte proliferation in drug-naïve pSS PBMC cultures (p<0.01) compared to mononuclear cell cultures alone. 1,25-dihydroxyvitamin D3 significantly decreased IFN- and IL-17 secreting Th cells in both drug naïve (p<0.005 and p<0.01, respectively) and treated subjects (p<0.05 and p<0.05, respectively) by increasing FoxP3 expressing CD4+CD25+ Treg cell frequency. Plasma B lymphocytes significantly reduced in the presence of 1,25-dihydroxyvitaminD3 in drug naïve pSS (p<0.001) and treated patients (p<0.05) mononuclear cell cultures compared to PBMC cultures alone. Total memory B cell subsets significantly increased with 1,25-dihydroxyvitaminD3 in drug naïve pSS when compared with PBMC cultures alone (p<0.005). IFN- and IL-17 cytokine levels in culture supernatants significantly reduced (p<0.05 and p<0.01, respectively) in drug naïve pSS patients' PBMC cultures with 1,25-dihydroxyvitaminD3, and IL-10 levels significantly enhanced in both drug-naïve (p<0.01) and treated pSS patients' PBMC cultures (p<0.01) in the presence of 1,25-dihydroxyvitaminD3. Conclusion:In conclusion, 1,25-dihydroxyvitaminD3 regulated immune responses in both treated and drug-naïve pSS patients, but have a more pronounced modulatory effect on mononuclear cell responses in drug-naive pSS patients.

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“…Moreover, both SS and CD pathologies are associated with an increased risk of lymphoma occurrence. Initially considered a T cell dysregulation, we recognized that the major derangement and dysregulation of the B lymphocytes in both peripheral circulation and glandular tissues of the SS patients plays a central part in the pathogenic processes[ 44 ]. The lymphoma risk is increased in SS patients especially for the marginal zone lymphoma, namely the parotid gland mucosa associated lymphoid tissue lymphoma, and the diffuse large B-cell lymphoma[ 45 ].…”

Section: Discussionmentioning

confidence: 99%

Celiac disease and Sjögren’s syndrome: A case report and review of literature

Balaban¹,

Mihai²,

Dima³

et al. 2020

WJCC

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BACKGROUND Celiac disease (CD) is a systemic, chronic immune-mediated disease triggered by gluten ingestion in genetically-susceptible individuals, with a prevalence of 1% worldwide. Sjogren's syndrome (SS) is also a systemic autoimmune disease, mainly characterized by ocular and oral sicca symptoms and signs. Sharing a common genetic background, CD and SS are known associated autoimmune diseases, but currently available guidelines are not reporting it. CASE SUMMARY We report the case of a 39-year-old woman, who was in the care of her rheumatologist for 2 years with SS. On routine follow-up she was found to have iron deficiency, without anemia. She had no gastrointestinal complaints and denied any obvious source of blood loss. IgA tissue transglutaminase antibodies were positive and endoscopy with duodenal biopsies revealed crypt hyperplasia and villous atrophy. A diagnosis of CD was set and gluten-free diet was recommended. CONCLUSION We present a review of existing data in the literature regarding the association of the two diseases, summarizing prevalence studies of CD in SS patients and the other way around. Screening recommendations and future research perspectives are also discussed, highlighting clinically relevant unanswered questions with respect to the association of CD with SS.

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B cell dysregulation in primary Sjögren’s syndrome: A review

Cited by 49 publications

References 90 publications

Current State of Knowledge on Primary Sjögren’s Syndrome, an Autoimmune Exocrinopathy

Current State of Knowledge on Primary Sjögren’s Syndrome, an Autoimmune Exocrinopathy

1,25-dihydroxyvitamin D3 regulates t helper and b lymphocyte responses substantially in drug-naive primary Sjögren’s syndrome patients’ mononuclear cells

Celiac disease and Sjögren’s syndrome: A case report and review of literature

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