ArticleArthritis and rheumatism2011
The NZM2410-derived lupus susceptibility locus Sle2c1 increases Th17 polarization and induces nephritis in fas-deficient mice.
Article in Arthritis and rheumatism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- The Role of B1 Cells in Systemic Lupus Erythematosus.Frontiers in immunology · 2022Review
- A Variant of sNASP Exacerbates Lymphocyte Subset Disorder and Nephritis in a Spontaneous Lupus Model Sle1.Yaa Mouse.Mediators of inflammation · 2021Article
- A Variant of the Histone-Binding Protein sNASP Contributes to Mouse Lupus.Frontiers in immunology · 2019Article
- Relative Contributions of B Cells and Dendritic Cells from Lupus-Prone Mice to CD4Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- A Skint6 allele potentially contributes to mouse lupus.Genes and immunity · 2017Article
- BAFF Induces Tertiary Lymphoid Structures and Positions T Cells within the Glomeruli during Lupus Nephritis.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- B cell contribution of the CD4Autoimmunity · 2017Review
- Glucose Oxidation Is Critical for CD4+ T Cell Activation in a Mouse Model of Systemic Lupus Erythematosus.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Contribution of B-1a cells to systemic lupus erythematosus in the NZM2410 mouse model.Annals of the New York Academy of Sciences · 2015Review
- Dysregulated CD4+ T cells from SLE-susceptible mice are sufficient to accelerate atherosclerosis in LDLr-/- mice.Annals of the rheumatic diseases · 2015Article
- Normalization of CD4+ T cell metabolism reverses lupus.Science translational medicine · 2015Article
- Association between leptin and systemic lupus erythematosus.Rheumatology international · 2014Review
- P2X7 blockade attenuates murine lupus nephritis by inhibiting activation of the NLRP3/ASC/caspase 1 pathway.Arthritis and rheumatism · 2013Article
- The combination of two Sle2 lupus-susceptibility loci and Cdkn2c deficiency leads to T-cell-mediated pathology in B6.Fas(lpr) mice.Genes and immunity · 2013Article
- The granulocyte colony stimulating factor pathway regulates autoantibody production in a murine induced model of systemic lupus erythematosus.Arthritis research & therapy · 2013Article
- Cyclin-dependent kinase inhibitor Cdkn2c deficiency promotes B1a cell expansion and autoimmunity in a mouse model of lupus.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Megakaryocyte progenitors are the main APCs inducing Th17 response to lupus autoantigens and foreign antigens.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Role of MHC-linked susceptibility genes in the pathogenesis of human and murine lupus.Clinical & developmental immunology · 2012Review
- Cyclin-dependent kinase inhibitor Cdkn2c regulates B cell homeostasis and function in the NZM2410-derived murine lupus susceptibility locus Sle2c1.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- A New Zealand Black-derived locus suppresses chronic graft-versus-host disease and autoantibody production through nonlymphoid bone marrow-derived cells.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveSle2 is a lupus susceptibility locus that has been linked to glomerulonephritis in the NZM2410 mouse. By itself, Sle2 does not induce any autoimmune pathology but results in the accumulation of B-1a cells. This study was designed to assess the contribution of Sle2 to the pathogenesis of autoimmunity.
methodsSle2 or its subcongenic intervals (Sle2a, Sle2b, and Sle2c1) were bred to Fas-deficient B6.lpr mice. Lymphoid phenotypes, which were focused on T cells, were assessed by flow cytometry, and histopathologic changes were compared between cohorts of B6.Sle2.lpr congenic mice and B6.lpr mice of ages up to 6 months.
resultsSle2 synergized with lpr, resulting in a greatly accelerated lymphadenopathy that largely targeted T cells and mapped to the Sle2c1 locus. This locus has been identified as the main contributor to B-1a cell expansion. Further analyses showed that Sle2c1 expression skewed the differentiation and polarization of Fas-deficient T cells, with a reduction of the CD4+CD25+FoxP3+ regulatory T cell subset and an expansion of the Th17 cells. This was associated with a high number of T cell infiltrates that promoted severe nephritis and dermatitis in the B6.Sle2c1.lpr mice.
conclusionThese results show that Sle2c1 contributes to lupus pathogenesis by affecting T cell differentiation in combination with other susceptibility loci, such as lpr. The significance of the cosegregation of this phenotype and B-1a cell expansion in Sle2c1-expressing mice in relation to the pathogenesis of lupus is discussed.
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