ReviewFrontiers in immunology2024
Subpopulation dynamics of T and B lymphocytes in Sjögren's syndrome: implications for disease activity and treatment.
Review in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed.
- Ophthalmic Treatments and Evolving Management of Sjögren's Disease: An Overview.Journal of clinical medicine · 2026Review
- Overlap syndrome between sarcoidosis and Sjögren's disease presenting as hypopituitarism: case report and review of literature.Endocrine journal · 2026Review
- Autoimmune Diseases and the Vestibular and Oculomotor System: Clinical Presentation, Diagnosis, and Treatment.Journal of eye movement research · 2026Review
- Molecular Insights into Oral Manifestations in Sjögren's Disease.International journal of molecular sciences · 2026Review
- Diet and Medicinal Herbs as Adjunctive Approaches to Immune Homeostasis in Sjögren's Disease.International journal of molecular sciences · 2026Review
- IL-2: a promising topical treatment for Sjögren's disease-related dry eye disease.Arthritis research & therapy · 2026Article
- Advances in nanotechnology for the diagnosis and management of autoimmune diseases.Asian journal of pharmaceutical sciences · 2026Review
- Chest muscle area, spleen density, CD4 + T%, and C4 to predict the development of interstitial lung disease in patients with Sjögren's syndrome: a clinical prediction model.Clinical rheumatology · 2026Article
- FASN-mediated metabolic reprogramming drives CD4Arthritis research & therapy · 2026Article
- Autoimmune nodopathy associated with Sjögren's disease and nephrotic syndrome: a case report and literature review.Frontiers in immunology · 2026Review
- Dysregulated expression of PSGL-1 and ADAM8 in Sjögren's disease: potential contribution to disease pathogenesis.Frontiers in immunology · 2026Article
- Macrophage polarization in Sjögren's syndrome: from mechanisms to therapeutic translation.Frontiers in immunology · 2026Review
- Pauci-Immune Crescentic Glomerulonephritis Associated With Primary Sjögren Syndrome: A Case Report.Cureus · 2026Article
- Tissue-Specific Expansion of Age-Associated B Cells via IFN-γ and IL-21 Within Salivary Glands in Sjögren Disease.Journal of immunology research · 2026Article
- Immune microenvironment dynamics in pregnant patients with concomitant autoimmune diseases: mechanisms, challenges, and clinical significance.Military Medical Research · 2026Review
- Regulatory T cells in primary sjögren disease: regulatory mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
- Clinical applications and challenges of CD40/CD40L signaling regulation in autoimmune diseases.Frontiers in immunology · 2026Review
- Oral Manifestations of Sjögren's Syndrome: Recognition, Management, and Interdisciplinary Care.Medicina (Kaunas, Lithuania) · 2025Review
- Nitrate Prevents Sjögren's Disease by Modulating T Helper Cells via NF-κB Pathway Suppression.Oral diseases · 2025Article
- Associations Between Th17 Cell Markers (IL-23R, CCR6, and IL-17) and Clinical Profiles in Sjögren's Disease.Diagnostics (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sjögren's syndrome (SS) is an autoimmune disorder primarily affecting the body's exocrine glands, particularly the salivary and lacrimal glands, which lead to severe symptoms of dry eyes and mouth. The pathogenesis of SS involves the production of autoantibodies by activated immune cells, and secretion of multiple cytokines, which collectively lead to tissue damage and functional impairment. In SS, the Immune interaction among T and B cells is particularly significant. Lymphocytic infiltration in the salivary glands is predominantly composed of CD4+ T cells, whose activation cause the death of glandular epithelial cells and subsequent tissue destruction. The excessive activity of T cells contributes significantly to the disease mechanism, with helper T cells (CD4+) differentiating into various subgroups including Th1/Th2, Th17, as well as Treg, each contributing to the pathological process through distinct cytokine secretion. In patients with SS, B cells are excessively activated, leading to substantial production of autoantibodies. These antibodies can attack self-tissues, especially the lacrimal and salivary glands, causing inflammation and tissue damage. Changes in B cell subpopulations in SS patients, such as increases in plasmablasts and plasma cells, correlate positively with serum autoantibody levels and disease progression. Therapies targeting T cells and B cells are extensively researched with the aim of alleviating symptoms and improving the quality of life for patients. Understanding how these cells promote disease development through various mechanisms, and further identifying novel T and B cell subgroups with functional characterization, will facilitate the development of more effective strategies to treat SS.
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