Dendritic cells, T-cells and epithelial cells: a crucial interplay in immunopathology of primary Sjögren's syndrome

Hillen, Maarten R; Ververs, Francesca A.; Kruize, Aike A.; Roon, J.A. van

doi:10.1586/1744666x.2014.878650

Cited by 40 publications

(23 citation statements)

References 76 publications

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“…Lacrimal gland biopsy, which shows a 75% involvement from CD4 T cells, supports the theory that T cells play a significant role in the generation and perpetuation of inflammatory infiltrates in salivary glands in SS [14,15]. The autoantigens expressed on the surface of endothelial cells may trigger the T cell migration into the lacrimal gland tissue and then, with the association with cell adhesion molecules, be directed to the tissue expressing the antigens.…”

Section: Review Of the Known Pathogenesis Of Sjögren Syndromesupporting

confidence: 65%

Untitled

2016

OCR

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Section: Review Of the Known Pathogenesis Of Sjögren Syndromesupporting

confidence: 65%

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2016

OCR

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“…15 Interactions among glandular vascular endothelial cells, glandular epithelial cells, and dendritic cells drive the immune response. 1,15,19 Recruitment and activation of T and B cells by HLA-DRrestricted antigen-presenting cells leads to generation of memory lymphocytes and plasma cells that produce autoantibodies (especially to SS-A and SS-B antigens). 15 Dysfunction or depletion of specific T cell subsets (e.g., T regulatory cells 20 and follicular T helper cells 21,22 ) may also be involved in the pathogenesis.…”

Section: Pathogenesis Of Sjogren's Syndromementioning

confidence: 99%

Pulmonary and Bronchiolar Involvement in Sjogren's Syndrome

Chung

Wilgus

Fishbein

et al. 2019

Semin Respir Crit Care Med

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Sjogren's syndrome (SS) is a chronic autoimmune disease characterized by mononuclear cells (principally lymphocytes) infiltrating exocrine glands (e.g., salivary and lacrimal glands), leading to destruction of exocrine epithelial cells and dryness of mucosal surfaces. Cardinal symptoms are dry eyes (xerophthalmia) and dry mouth (xerostomia). Extraglandular sites are affected in 30 to 40% of cases of SS (particularly neurological, kidneys, skin, and lungs). B cell hyperactivity, autoantibody production, and hypergammaglobulinemia are cardinal features of SS. Primary SS is not associated with other autoimmune diseases. However, SS can complicate diverse autoimmune disorders (particularly systemic lupus erythematosus, rheumatoid arthritis, and scleroderma); this form is termed “secondary SS.” Pulmonary involvement is usually not a dominant feature of SS, but may be severe in some cases. In this review, we discuss specific tracheal, bronchiolar, and pulmonary complications of SS including xerotrachea, bronchiolitis, bronchiectasis, interstitial lung disease, nonspecific interstitial pneumonia, usual interstitial pneumonia, lymphoid interstitial pneumonia, organizing pneumonia, acute fibrinous and organizing pneumonia, pulmonary cysts, pleural effusions, pulmonary amyloidosis, and bronchus- or lung-associated lymphomas.

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“…Induced models include ro-peptideinduced or murine cytomegalovirus CMV-induced pSS. [80][81][82][83][84] Btk knockout or inhibition has yet to be studied in the context of pSS. However, based on the ability of Btk inhibition to decrease autoantibody production and inhibit myeloid type I IFN responses in other disease models, a rationale to study the role of Btk in pSS is readily apparent.…”

Section: Sjögren's Syndromementioning

confidence: 99%

Bruton’s tyrosine kinase in chronic inflammation: from pathophysiology to therapy

Hartkamp¹,

Reedquist

2015

IJICMR

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Bruton's tyrosine kinase (Btk) not only plays a role in differentiation and activation of B-cells but is also involved in regulating signaling in myeloid cell populations, mast cells, platelets, and osteoclasts. Btk plays a critical role in B-cell receptor signaling and has been shown to be involved in CD40 ligation, Toll-like receptor triggering, and Fc-receptor signaling as well, suggesting that targeting Btk might be particularly useful in autoimmune diseases characterized by pathologic antibodies, macrophage activation, and myeloid-derived type I interferon responses. Btk knockout and X-linked immunodeficiency mouse material and X-linked agammaglobulinemia patient samples are powerful tools to examine the role of Btk in health and disease. In addition, the recent development of several covalent and noncovalent small-molecule inhibitors specifically targeting Btk can contribute to our understanding of the functional role of Btk in several cell types and disease mechanisms. Specific Btk inhibitors have been used in both in vitro and in vivo models for autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, systemic sclerosis, and Sjögren's syndrome. The current small-molecule Btk inhibitors have demonstrated potent and selective Btk inhibition in preclinical studies, and some inhibitors have propelled the clinical development of such molecules toward clinical trials in patients with rheumatoid arthritis. Future studies on the effectiveness of Btk inhibition in other autoimmune diseases could further broaden the understanding of the disease mechanisms as well as lead to new targeted therapies.

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Dendritic cells, T-cells and epithelial cells: a crucial interplay in immunopathology of primary Sjögren's syndrome

Cited by 40 publications

References 76 publications

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Pulmonary and Bronchiolar Involvement in Sjogren's Syndrome

Bruton’s tyrosine kinase in chronic inflammation: from pathophysiology to therapy

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Dendritic cells, T-cells and epithelial cells: a crucial interplay in immunopathology of primary Sjögren's syndrome

Cited by 40 publications

References 76 publications

Untitled

Untitled

Pulmonary and Bronchiolar Involvement in Sjogren's Syndrome

Bruton&rsquo;s tyrosine kinase in chronic inflammation: from pathophysiology to therapy

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Bruton’s tyrosine kinase in chronic inflammation: from pathophysiology to therapy