Unique Phenotypes and Functions of Follicular Helper T Cells and Regulatory T Cells in Sjögren’s Syndrome

Saitō, Masako; Otsuka, Kunihiro; Ushio, Aya; Yamada, Akiko; Arakaki, Rieko; Kudo, Yasusei; Ishimaru, Naozumi

doi:10.2174/1573397113666170125122858

Cited by 27 publications

(28 citation statements)

References 110 publications

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“…Sjögren syndrome can appear independently of other conditions as a primary disease (primary Sjögren syndrome) or manifest itself secondarily as a late complication with sicca symptoms (secondary Sjögren syndrome) in the presence of other systemic conditions, such as rheumatoid arthritis, systemic lupus erythematosus, or scleroderma [149,150]. In Sjögren syndrome affected tissues, several subsets of B and T cells can be identified, predominantly consisting of CD4+ T helper cell subtypes, such as Th1, Th17, and Tfh cells [151]. The interaction between epithelial cells, dendritic cells, and B and T cells results in an increased production of Tfh and Th17 cells, which intensifies the inflammation and increases autoantibody production [152].…”

Section: Th17/il-17 In Immunoprotection and Immunopathologymentioning

confidence: 99%

Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases

Bunte

Beikler

2019

IJMS

341

290

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Innate immunity represents the semi-specific first line of defense and provides the initial host response to tissue injury, trauma, and pathogens. Innate immunity activates the adaptive immunity, and both act highly regulated together to establish and maintain tissue homeostasis. Any dysregulation of this interaction can result in chronic inflammation and autoimmunity and is thought to be a major underlying cause in the initiation and progression of highly prevalent immune-mediated inflammatory diseases (IMIDs) such as psoriasis, rheumatoid arthritis, inflammatory bowel diseases among others, and periodontitis. Th1 and Th2 cells of the adaptive immune system are the major players in the pathogenesis of IMIDs. In addition, Th17 cells, their key cytokine IL-17, and IL-23 seem to play pivotal roles. This review aims to provide an overview of the current knowledge about the differentiation of Th17 cells and the role of the IL-17/IL-23 axis in the pathogenesis of IMIDs. Moreover, it aims to review the association of these IMIDs with periodontitis and briefly discusses the therapeutic potential of agents that modulate the IL-17/IL-23 axis.

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Section: Th17/il-17 In Immunoprotection and Immunopathologymentioning

confidence: 99%

Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases

Bunte

Beikler

2019

IJMS

341

290

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“…During pathology, SGEC induce activation and differentiation of T helper to T follicular helper by the release of IL6 and ICOS ligand expression. The activated follicular cells in turn secrete IL-21 cytokine which mediates B cell maturation and proliferation [ 131 ]. In conclusion, the combined activation of T-cell subtypes creates an optimal environment for detrimental B cell activation and the breakdown of tolerance.…”

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

106

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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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“…pSS is considered to be essentially driven by a complex interaction between epithelial barrier and adaptive and innate immunity. Macrophages, dendritic cells, NK cells, T cells (Th1, Th2, Th17, Tfh, Tfr, Treg) and B cells have been reported to be involved in the pathogenesis of the disease (3)(4)(5)(6). Additionally, our previous work has clari ed the essential role of MDSCs in the progression of pSS (7).…”

Section: Introductionmentioning

confidence: 91%

Mesenchymal stem cell enhances the function of MDSCs in experimental Sjögren syndrome mice

Tian

Hong

Zhu

et al. 2020

Preprint

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Background Primary Sjögren’s syndrome (pSS) is a chronic systemic autoimmune disease characterized by lymphocytic infiltrates in exocrine glands. Mesenchymal stem cells (MSCs) have been proved to be effective in the treatment of different autoimmune diseases. Although MSC transplantation has been demonstrated to be an effective therapeutic approach to treat SS, the underlying mechanisms are still elusive. Our previous study has identified the reduced suppressive capacity of MDSCs advanced the progression of experimental Sjögren’s syndrome (ESS). Methods The ESS mouse model was induced with murine salivary glands proteins emulsified in an equal volume of Freund’s adjuvant. Both frequency and phenotype of MDSCs during ESS development in mice were analyzed by flow cytometry. The suppressive capacity of MDSCs was examined by CD4+ T cell proliferation test, CFSE-labelled CD4+ T cell was analyzed by flow cytometry. Both phenotype and function of MDSCs upon MSCs treatment were analyzed in vitro and in vivo. The function of MSCs in modulating the suppressive function of MDSCs was further evaluated by silencing TGF-β in MSCs. Results In this study, we found that BM-MSCs significantly enhanced the suppressive function of MDSCs (PMN-MDSCs/M-MDSCs) with high levels of Arginase and NO, decreased the levels of CD40, CD80, CD86 and MHC-II expression on MDSCs, thus attenuating the disease progression in ESS mice. Furthermore, the enhanced suppressive function of MDSCs was mediated by BM-MSC-secreted TGF-β, and the therapeutic effect of BM-MSCs in inhibiting ESS was almost abolished after silencing TGF-β in BM-MSCs. Conclusions Taken together, our results demonstrated that BM-MSCs alleviated the ESS progression by up-regulating the immunosuppressive effect of MDSCs through TGF-β/Smad pathway, offering a novel mechanism for MSCs in the treatment of pSS.

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Unique Phenotypes and Functions of Follicular Helper T Cells and Regulatory T Cells in Sjögren’s Syndrome

Cited by 27 publications

References 110 publications

Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases

Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases

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

Mesenchymal stem cell enhances the function of MDSCs in experimental Sjögren syndrome mice

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