ArticleJournal of clinical immunology2012
B-cell tolerance defects in the B6.Aec1/2 mouse model of Sjögren's syndrome.
Article in Journal of clinical immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- B-Cell Receptor Repertoire: Recent Advances in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2024Review
- Autoimmune B Cell Repertoire in a Mouse Model of Sjögren's Syndrome.Frontiers in immunology · 2021Article
- Differentially Expressed Gene Pathways in the Conjunctiva of Sjögren Syndrome Keratoconjunctivitis Sicca.Frontiers in immunology · 2021Article
- Fingolimod reduces salivary infiltrates and increases salivary secretion in a murine Sjögren's model.Journal of autoimmunity · 2020Article
- The Pathophysiology of Dry Eye Disease: What We Know and Future Directions for Research.Ophthalmology · 2017Review
- Mechanisms of central tolerance for B cells.Nature reviews. Immunology · 2017Review
- TLR9 promotes tolerance by restricting survival of anergic anti-DNA B cells, yet is also required for their activation.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- The T cell in Sjogren's syndrome: force majeure, not spectateur.Journal of autoimmunity · 2012Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
purposePrimary Sjögren's syndrome (SjS) is an autoimmune disorder characterized by lymphocytic infiltration of the salivary and lacrimal glands, B-cell clonal expansions and an increased risk of lymphoma. In order to understand the role of B cells in this disorder, the antibody repertoire and B-cell maturation were studied in a mouse model of SjS called B6.Aec1/2.
methodsB6.Aec1/2 serum was analyzed for antibodies by ELISA and immunoprecipitation, B-cell development by flow cytometry, and antibody gene rearrangements by CDR3 spectratyping and quantitative PCR. In order to test the functional consequences of the observed defects, B6.Aec1/2 mice were crossed with anti-dsDNA antibody heavy chain knock-in mice (B6.56R).
resultsB6.Aec1/2 mice exhibit B-cell clonal expansions, have altered serum immunoglobulin levels and spontaneously produce multireactive autoantibodies. B6.Aec1/2 mice also have decreased numbers of bone marrow pre-B cells and decreased frequencies of kappa light chain gene deletion. These findings suggest that B6.Aec1/2 mice have a defective early B-cell tolerance checkpoint. B6.56R.Aec1/2 mice unexpectedly had lower anti-dsDNA antibody levels than B6.56R mice and less salivary gland infiltration than B6.Aec1/2 mice.
conclusionsThese data suggest that the early tolerance checkpoint defect in B6.Aec1/2 mice is not sufficient to promulgate disease in mice with pre-formed autoantibodies, such as B6.56R. Rather, B6.Aec1/2 mice may require a diverse B-cell repertoire for efficient T-B-cell collaboration and disease propagation. These findings imply that therapies aimed at reducing B-cell diversity or T-B interactions may be helpful in treating SjS.
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Registered trials
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