ArticleJournal of immunology (Baltimore, Md. : 1950)2007
Development of Sjogren's syndrome in nonobese diabetic-derived autoimmune-prone C57BL/6.NOD-Aec1Aec2 mice is dependent on complement component-3.
Article in Journal of immunology (Baltimore, Md. : 1950), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 46 citations in OpenAlex.
- Review
- Advances and prospects of platelet-rich plasma therapy in veterinary ophthalmology.Veterinary research communications · 2023Review
- Marginal Zone B (MZB) Cells: Comparison of the Initial Identification of Immune Activity Leading to Dacryoadenitis and Sialadenitis in Experimental Sjögren's Syndrome.International journal of molecular sciences · 2023Article
- Optimization of a Plasma Rich in Growth Factors Membrane for the Treatment of Inflammatory Ocular Diseases.Bioengineering (Basel, Switzerland) · 2022Article
- A MZB Cell Activation Profile Present in the Lacrimal Glands of Sjögren's Syndrome-Susceptible C57BL/6.NOD-International journal of molecular sciences · 2022Article
- Current experimental methods to investigate the impact of specialized pro-resolving lipid mediators on Sjögren's syndrome.Frontiers in immunology · 2022Review
- The Involvement of Innate and Adaptive Immunity in the Initiation and Perpetuation of Sjögren's Syndrome.International journal of molecular sciences · 2021Review
- Innate Immunity and Biological Therapies for the Treatment of Sjögren's Syndrome.International journal of molecular sciences · 2020Review
- Testosterone Influence on Gene Expression in Lacrimal Glands of Mouse Models of Sjögren Syndrome.Investigative ophthalmology & visual science · 2019Article
- B cells in the pathogenesis of primary Sjögren syndrome.Nature reviews. Rheumatology · 2018Review
- Myd88 is required for disease development in a primary Sjögren's syndrome mouse model.Journal of leukocyte biology · 2017Article
- Myeloid Populations in Systemic Autoimmune Diseases.Clinical reviews in allergy & immunology · 2017Review
- What can Sjögren's syndrome-like disease in mice contribute to human Sjögren's syndrome?Clinical immunology (Orlando, Fla.) · 2017Review
- Multiple Roles for B-Lymphocytes in Sjogren's Syndrome.Journal of clinical medicine · 2016Review
- AT-RvD1 combined with DEX is highly effective in treating TNF-α-mediated disruption of the salivary gland epithelium.Physiological reports · 2016Article
- Age-related Defects in Ocular and Nasal Mucosal Immune System and the Immunopathology of Dry Eye Disease.Ocular immunology and inflammation · 2016Review
- Targeting of Ly9 (CD229) Disrupts Marginal Zone and B1 B Cell Homeostasis and Antibody Responses.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Tear proteomic analysis of Sjögren syndrome patients with dry eye syndrome by two-dimensional-nano-liquid chromatography coupled with tandem mass spectrometry.Scientific reports · 2014Article
- Interleukin-7 enhances the Th1 response to promote the development of Sjögren's syndrome-like autoimmune exocrinopathy in mice.Arthritis and rheumatism · 2013Article
- Transient depletion of CD4+ CD25+ regulatory T cells results in multiple autoimmune diseases in wild-type and B-cell-deficient NOD mice.Immunology · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
The role of complement in the etiology of Sjögren's syndrome (SjS), a human autoimmune disease manifested primarily by salivary and lacrimal gland dysfunction resulting in dry mouth/dry eye syndrome, remains ill-defined. In the present study, we examined the role of complement component-3 (C3) using a newly constructed C3-gene knockout mouse, C57BL/6.NOD-Aec1Aec2.C3(-/-). Inactivation of C3 in the parental C57BL/6.NOD-Aec1Aec2 strain, a model of primary SjS, resulted in a diminished or total absence of both preclinical and clinical manifestations during development and onset of disease, including reduced acinar cell apoptosis, reduced levels of caspase-3, lack of leukocyte infiltration of submandibular glands, reduced synthesis of disease-associated autoantibodies, maintenance of normal glandular architecture, and retention of normal saliva secretion. In addition, C57BL/6-NOD.Aec1Aec2.C3(-/-) mice did not exhibit increased numbers of marginal zone B cells, a feature of SjS-prone C57BL/6-NOD.Aec1Aec2 mice. Interestingly, C57BL/6-NOD.Aec1Aec2.C3(-/-) mice retained some early pathological manifestations, including activation of serine kinases with proteolytic activity for parotid secretory protein. This improvement in the clinical manifestations of SjS-like disease in C57BL/6.NOD-Aec1Aec2.C3(-/-) mice, apparently a direct consequence of C3 deficiency, supports a much more important role for complement in the adaptive autoimmune response than previously recognized, possibly implicating an essential role for innate immunity.
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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.