ReviewJournal of autoimmunity2012
The T cell in Sjogren's syndrome: force majeure, not spectateur.
Review in Journal of autoimmunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.
- Composition and regulation of the immune microenvironment of salivary gland in Sjögren's syndrome.Frontiers in immunology · 2022Pooled it
- Persistence and selection of an expanded B-cell clone in the setting of rituximab therapy for Sjögren's syndrome.Arthritis research & therapy · 2014Trial
- Therapeutic effects of a synthetic glabridin derivative on metabolic immuno-regulation and salivary gland functional restoration in experimental Sjögren's syndrome.Experimental & molecular medicine · 2026Article
- A CD4Nature communications · 2026Article
- mTOR signaling pathway in primary Sjögren's syndrome: Pathogenesis and potential therapeutic targets (Review).International journal of molecular medicine · 2026Review
- Regulatory T cells in primary sjögren disease: regulatory mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
- Development of an improved preclinical humanized mouse platform representing the diverse clinical phenotypes of Sjögren's syndrome.Frontiers in immunology · 2026Article
- ACSL5 programs fatty acid metabolism and mitochondrial fitness to sustain pathogenic T cells and exacerbate Sjögren's syndrome.International journal of biological sciences · 2026Article
- Recent insights into the roles and therapeutic potentials of GLS1 in inflammatory diseases.Journal of pharmaceutical analysis · 2025Review
- Regulatory Role of FGL-1 in Interorgan Communication by Controlling T Cell Homeostasis During the Onset of Sjögren Disease.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Mitochondrial dysfunction and fatigue in Sjögren's disease.RMD open · 2025Article
- Lipid Metabolism: An Emerging Player in Sjögren's Syndrome.Clinical reviews in allergy & immunology · 2025Review
- Biological functions and affected signaling pathways by Long Non-Coding RNAs in the immune system.Non-coding RNA research · 2025Review
- USP18-mediated protein stabilization of NOTCH1 is associated with altered Th17/Treg cell ratios and B cell-mediated autoantibody secretion in Sjögren syndrome.Immunologic research · 2024Article
- The impact of alternate-day fasting on the salivary gland stem cell compartments in non-obese diabetic mice with newly established Sjögren's syndrome.Biochimica et biophysica acta. Molecular cell research · 2024Article
- Endometriosis and Sjögren's syndrome: Bidirectional associations in population-based 15-year retrospective cohorts.Acta obstetricia et gynecologica Scandinavica · 2024Article
- Immunometabolic alteration of CD4Clinical and experimental medicine · 2024Article
- Inhibition of JAK-STAT pathway corrects salivary gland inflammation and interferon driven immune activation in Sjögren's disease.Annals of the rheumatic diseases · 2024Article
- IL-27 promotes pathogenic T cells in a mouse model of Sjögren's disease.Clinical immunology (Orlando, Fla.) · 2024Article
- Literature mining discerns latent disease-gene relationships.Bioinformatics (Oxford, England) · 2024Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Sjogren's syndrome (SS) is characterized by infiltration of exocrine glands with T and B lymphocytes, leading to glandular dysfunction and frequently accompanied by hypergammaglobulinemia and autoantibodies. The role of T cells, which predominate in the lesions, has attracted much interest. CD4 T cells seem to be responding to autoantigens on apoptotic cells, such as the Ro and La antigens, or to the cytoskeletal antigen α-fodrin. Physical injury to ocular surfaces may also lead to T cell mediated responses to self antigens and perpetuate disease. Within the salivary glands, T cell responsiveness is further promoted by the special capacity of salivary epithelial tissue to provide costimulation and enhanced antigen presentation. Cytokines are key mediators of the T cell contribution to pathology, with roles attributed both to Th1 and Th2 cells. Recently, striking data implicate Th17 cells in the stimulation of B cells, and a role for the related cytokine IL-21 produced by follicular T helper cells is now appreciated. Dysfunction of T regulatory cells has been shown to have a role in the exuberant production of cytokines by Th17 cells. Beyond their role in provoking B cell hyperactivity and immunoglobulin secretion, T cells are directly involved in destruction of glands through Fas and perforin-mediated cytotoxicity. Animal models of SS have confirmed the role of T cell derived cytokines in disease and support a role for effector-memory cells in pathogenesis. Further elucidation of the role of T cells will open avenues for better treatment of SS, whose current management is still mainly supportive.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.