ArticleArthritis and rheumatism2013
Protein kinase Cβ is required for lupus development in Sle mice.
Article in Arthritis and rheumatism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Interferon and B-cell Signatures Inform Precision Medicine in Lupus Nephritis.Kidney international reports · 2024Article
- Iguratimod represses B cell terminal differentiation linked with the inhibition of PKC/EGR1 axis.Arthritis research & therapy · 2019Article
- PKK deficiency in B cells prevents lupus development in Sle lupus mice.Immunology letters · 2017Article
- Support for phosphoinositol 3 kinase and mTOR inhibitors as treatment for lupus using in-silico drug-repurposing analysis.Arthritis research & therapy · 2017Article
- Lupus pathobiology based on genomics.Immunogenetics · 2017Review
- Genetics and pathogenesis of systemic lupus erythematosus and lupus nephritis.Nature reviews. Nephrology · 2015Review
- Mechanisms of Kidney Injury in Lupus Nephritis - the Role of Anti-dsDNA Antibodies.Frontiers in immunology · 2015Review
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
objectiveTo evaluate the requirement for protein kinase Cβ (PKCβ) in the development of lupus in mice, and to explore the potential of targeting PKCβ as a therapeutic strategy in lupus.
methodsCongenic mice bearing the disease loci Sle1 or Sle1 and Sle3, which represent different stages of severity in the development of lupus, were crossed with PKCβ-deficient mice. The effect of PKCβ deficiency in lupus development was analyzed. In addition, the effects of the PKCβ-specific inhibitor enzastaurin on the survival of B cells from mice with lupus and human 9G4-positive B cells as well as the in vivo effect of enzastaurin treatment on the development of lupus in Sle mice were investigated.
resultsIn Sle mice, PKCβ deficiency abrogated lupus-associated phenotypes, including high autoantibody levels, proteinuria, and histologic features of lupus nephritis. Significant decreases in spleen size and in the peritoneal B-1 cell population, reduced numbers of activated CD4 T cells, and normalized CD4:CD8 ratios were observed. PKCβ deficiency induced an anergic B cell phenotype and preferentially inhibited autoreactive plasma cells and autoantibodies in mice with lupus. Inhibition of PKCβ enhanced apoptosis of both B cells from Sle mice and human autoreactive B cells (9G4 positive). Treatment of Sle mice with the PKCβ-specific inhibitor enzastaurin prevented the development of lupus.
conclusionThis study identifies PKCβ as a central mediator of lupus pathogenesis, suggesting that PKCβ represents a promising therapeutic target for the treatment of systemic lupus erythematosus. Moreover, the results indicate the feasibility of using a PKCβ inhibitor for the treatment of lupus.
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