ArticleArthritis and rheumatism2008
Regulation of B cell tolerance by 129-derived chromosome 1 loci in C57BL/6 mice.
Article in Arthritis and rheumatism, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 14 citations in OpenAlex.
- Enhanced auto-antibody production and Mott cell formation in FcμR-deficient autoimmune mice.International immunology · 2014Article
- Article
- Characterization of Ly108 in the thymus: evidence for distinct properties of a novel form of Ly108.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
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6 authors at 1 institution in 1 country.
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Abstract
objectiveSystemic lupus erythematosus is a multifactorial disease with a strong genetic component. Previous studies have shown that a 129-derived chromosome 1 interval (Sle16) on the C57BL/6 (B6) background is sufficient to induce humoral autoimmunity. The aim of the present study was to elucidate the mechanisms by which this locus contributes to the loss of peripheral tolerance.
methodsAnti-single-stranded DNA (anti-ssDNA)-knockin transgenic mice (V(H)3H9R/Vkappa8R and V(H)3H9R) were crossed with a B6 congenic line named B6.129chr1b that carries the Sle16 locus. A parallel study of a gene-targeted animal, whose mutated gene is located within the 129chr1b interval on chromosome 1, was also performed.
resultsThe combination of V(H)3H9R/Vkappa8R with the 129chr1b interval resulted in impaired B cell anergy, and transgenic IgM and IgG anti-ssDNA antibodies were found in the circulation. The presence of IgG2a(a) anti-ssDNA and IgM(a) anti-Sm antibodies in sera indicated that the autoreactive transgenic B cells underwent class switching and epitope spreading. The 129chr1b locus appeared to have a dominant effect, since transgenic antibodies were also detected in mice carrying a single allele. The gene-targeted animals showed a similar phenotype.
conclusionThe presence of a single 129chr1b locus on the B6 background impaired B cell anergy, prevented deletion of anti-DNA transgenic B cells, and induced receptor revision. The findings of this study also emphasize that the autoimmune phenotype observed in mice with targeted genes located on chromosome 1 may simply arise from epistatic interactions between the 129 and B6 parental strains.
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