ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Cyclin-dependent kinase inhibitor Cdkn2c deficiency promotes B1a cell expansion and autoimmunity in a mouse model of lupus.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- B-1a Cells, but Not Marginal Zone B Cells, Are Implicated in the Accumulation of Autoreactive Plasma Cells in Lyn-/- Mice.ImmunoHorizons · 2024Article
- Urinary Long Non-Coding RNA Levels as Biomarkers of Lupus Nephritis.International journal of molecular sciences · 2023Article
- Pla2g2a promotes innate Th2-type immunity lymphocytes to increase B1a cells.Scientific reports · 2022Article
- The Role of B1 Cells in Systemic Lupus Erythematosus.Frontiers in immunology · 2022Review
- Modulation of microbiome diversity and cytokine expression is influenced in a sex-dependent manner during aging.Frontiers in microbiomes · 2022Article
- Polygenic autoimmune disease risk alleles impacting B cell tolerance act in concert across shared molecular networks in mouse and in humans.Frontiers in immunology · 2022Review
- Synthetic secoisolariciresinol diglucoside (LGM2605) inhibits Libby amphibole fiber-induced acute inflammation in mice.Toxicology and applied pharmacology · 2019Article
- A Variant of the Histone-Binding Protein sNASP Contributes to Mouse Lupus.Frontiers in immunology · 2019Article
- Early Generated B-1-Derived B Cells Have the Capacity To Progress To Become Mantle Cell Lymphoma-like Neoplasia in Aged Mice.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- A Skint6 allele potentially contributes to mouse lupus.Genes and immunity · 2017Article
- Analysis of IgM antibody production and repertoire in a mouse model of Sjögren's syndrome.Journal of leukocyte biology · 2016Article
- Expansion of B-1a Cells with Germline Heavy Chain Sequence in Lupus Mice.Frontiers in immunology · 2016Article
- Article
- Contribution of B-1a cells to systemic lupus erythematosus in the NZM2410 mouse model.Annals of the New York Academy of Sciences · 2015Review
- A Conserved Gammaherpesvirus Cyclin Specifically Bypasses Host p18(INK4c) To Promote Reactivation from Latency.Journal of virology · 2015Article
- Genetic and cellular dissection of the activation of AM14 rheumatoid factor B cells in a mouse model of lupus.Journal of leukocyte biology · 2015Article
- Contributions of B cells to lupus pathogenesis.Molecular immunology · 2014Review
- Autoimmunity in 2012.Clinical reviews in allergy & immunology · 2013Review
- 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
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The lupus-prone NZM2410 mice present an expanded B1a cell population that we have mapped to the Sle2c1 lupus susceptibility locus. The expression of Cdkn2c, a gene encoding for cyclin-dependent kinase inhibitor p18(Ink4c) and located within Sle2c1, is significantly lower in B6.Sle2c1 B cells than in B6 B cells. To test the hypothesis that the B1a cell expansion in B6.Sle2c1 mice was due to a defective p18 expression, we analyzed the B1a cell phenotypes of p18-deficient C57BL/6 mice. We found a dose-dependent negative correlation between the number of B1a cells and p18 expression in B cells, with p18-deficient mice showing an early expansion of the peritoneal B1a cell pool. p18 deficiency enhanced the homeostatic expansion of B1a cells but not of splenic conventional B cells, and the elevated number of B6.Sle2c1 B1a cells was normalized by cyclin D2 deficiency. These data demonstrated that p18 is a key regulator of the size of the B1a cell pool. B6.p18(-/-) mice produced significant amounts of anti-DNA IgM and IgG, indicating that p18 deficiency contributes to humoral autoimmunity. Finally, we have shown that Sle2c1 increases lpr-associated lymphadenopathy and T cell-mediated pathology. B6.p18(-/-).lpr mice showed a greater lymphadenopathy than B6.Sle2c1.lpr mice, but their renal pathology was intermediate between that of B6.lpr and B6.Sle2c1.lpr mice. This indicated that p18-deficiency synergizes, at least partially, with lpr-mediated pathology. These results show that Cdkn2c contributes to lupus susceptibility by regulating the size of the B1a cell compartment and hence their contribution to autoimmunity.
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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.