ArticleInflammation2012
Destruction of salivary and lacrimal glands by Th1-polarized reaction in a model of secondary Sjögren's syndrome in lupus-prone female NZB × NZWF(1) mice.
Article in Inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Subpopulation dynamics of T and B lymphocytes in Sjögren's syndrome: implications for disease activity and treatment.Frontiers in immunology · 2024Review
- The Autoimmune Rheumatic Disease Related Dry Eye and Its Association with Retinopathy.Biomolecules · 2023Review
- A MZB Cell Activation Profile Present in the Lacrimal Glands of Sjögren's Syndrome-Susceptible C57BL/6.NOD-International journal of molecular sciences · 2022Article
- Exploiting the role of T cells in the pathogenesis of Sjögren's syndrome for therapeutic treatment.Frontiers in immunology · 2022Review
- Cytokine/Chemokine/Growth Factor Profiles Contribute to Understanding the Pathogenesis of the Salivary Gland Dysfunction in Euthyroid Hashimoto's Thyroiditis Patients.Mediators of inflammation · 2021Article
- Article
- Protective role of commensal bacteria in Sjögren Syndrome.Journal of autoimmunity · 2018Article
- Sjögren-Like Lacrimal Keratoconjunctivitis in Germ-Free Mice.International journal of molecular sciences · 2018Article
- Managing Sjögren's Syndrome and non-Sjögren Syndrome dry eye with anti-inflammatory therapy.Clinical ophthalmology (Auckland, N.Z.) · 2014Review
- T helper cytokines in dry eye disease.Experimental eye research · 2013Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T helper (Th)1/Th2 balance determines the direction of some kinds of autoimmune diseases. The involvement of acini areas by CD4(+) helper T(Th) cell subset in submandibular and lacrimal glands are largely unknown in secondary Sjögren's syndrome (sSjS) with systemic lupus erythematosus (SLE). Submandibular and lacrimal glands were examined immunopathologically in lupus-prone female NZB × NZW(B/W)F(1) mice, model for human sSjS with SLE. Dacryoadenitis and sialoadenitis with renal failure developed with age. Infiltration of lymphoid cells (lymphocytes and plasma cells) expanded from the periductal areas in striated ducts to the acini, and the isolated foci in the acini were observed in those organs. The destruction of duct and acini epithelium, including the myoepithelium, was induced by interferon (IFN)-γ(+) and IgG2a(+) lymphoid cells, but not by interleukin(IL)-4(+), IL-5(+), IL-13(+), and IgG1(+) lymphoid cells. Compared with IL-5 and IL-13, high values of IFN-γ were produced systemically at various ages. Also local expression of IFN-γ mRNA was higher than that of IL-4 mRNA. The result suggests that the acini destruction in submandibular and lacrimal glands may be induced by systemic and local Th1 cell dominant reactions in lupus-prone B/WF(1) mice with sSjS.
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Registered trials
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