We are analyzing https://link.springer.com/article/10.1007/s10875-013-9866-5.

Title:
Tumor Necrosis Factor Receptor-associated Factor 1 influences KRN/I-Ag7 Mouse Arthritis Autoantibody Production | Journal of Clinical Immunology
Description:
Purpose Recently, genomewide association analysis has revealed that the Tumor Necrosis Factor Receptor-associated factor 1-Complement 5 (TRAF1-C5) containing locus on chromosome 9 was associated with an increased risk for RA. Studies in model systems suggested that either gain- or loss-of-function TRAF1 mutations have immune effects that could plausibly lead to or exacerbate the arthritis phenotype. KRN/I-Ag7 (KxB/N) is a genetic mouse model of inflammatory arthritis. We aimed to assess the impact of TRAF1 deficiency on KRN/I-Ag7 mice. Methods We have bred KRN/I-Ag7 mice onto a TRAF1-deficient background and followed cohorts for the spontaneous appearance of arthritis. We have also transferred KxB/N serum to B6.I-Ag7 TRAF1KO recipients. In addition, systemic autoimmunity was induced through cGVH by injecting bm12 splenocytes into TRAF1KO recipient mice. Results TRAF1-deficient KRN/I-Ag7 mice spontaneously developed severe, progressive arthritis, comparable to that seen in TRAF1-intact KRN/I-Ag7 mice. However, the anti-GPI antibody titer was significantly lower in the former group. Interestingly, the TRAF1KO mice that had background levels of anti-GPI antibodies still showed severe arthritis, although with a brief delay compared to TRAF1 sufficient mice. In addition, TRAF1KO mice were fully susceptible to passive, serum transfer experiments. In another model of autoimmunity, TRAF1KO had no effect on cGVH autoantibodies production; nor was the response to an exogenous antigen impaired. Conclusion The pathogenesis of spontaneous KRN/I-Ag7 arthritis can largely proceed by TRAF1-independent pathways. The production of anti-GPI autoantibody, but not other autoantibody or antibody responses, was markedly impaired by TRAF1 deficiency. The spontaneous arthritis model in KRN mice appears to be much less antibody dependent than previously believed.
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Topics {✒️}

traf1-intact krn/i-ag7 mice krn/i-ag7 mouse arthritis bred krn/i-ag7 mice spontaneous krn/i-ag7 arthritis krn/i-ag7 mice cell receptor-induced tyrosine-phosphoproteins i-ag7 traf1ko recipients month download article/chapter augment autoantibody-induced arthritis krn/i-ag7 nf-κb alternative pathway organ-specific autoimmune disease anti-gpi antibody titer anti-double-stranded dna organ-specific disease provoked putative candidate-gene associations anti-gpi autoantibody traf1-deficient mice showed severe arthritis krn mouse model immune-mediated diseases genome-wide association studies constitutive nf-κb mei qing ji & robert krn mice appears anti-gpi antibodies traf1-deficient background full article pdf helpful mouse bleeding clinical immunology aims cell-independent spontaneous loss genetic mouse model privacy choices/manage cookies spontaneous arthritis model arthritis res ther enhanced tnf signaling traf1 sufficient mice pkn1-mediated phosphorylation autoantibody production traf1ko recipient mice arthritis critically dependent /bxn arthritis model cgvh autoantibodies production springer semin immun inflammatory cell infiltration article cheng autophagy-related genes related subjects rheumatoid arthritis rheumatoid arthritis

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         description:Recently, genomewide association analysis has revealed that the Tumor Necrosis Factor Receptor-associated factor 1-Complement 5 (TRAF1-C5) containing locus on chromosome 9 was associated with an increased risk for RA. Studies in model systems suggested that either gain- or loss-of-function TRAF1 mutations have immune effects that could plausibly lead to or exacerbate the arthritis phenotype. KRN/I-Ag7 (KxB/N) is a genetic mouse model of inflammatory arthritis. We aimed to assess the impact of TRAF1 deficiency on KRN/I-Ag7 mice. We have bred KRN/I-Ag7 mice onto a TRAF1-deficient background and followed cohorts for the spontaneous appearance of arthritis. We have also transferred KxB/N serum to B6.I-Ag7 TRAF1KO recipients. In addition, systemic autoimmunity was induced through cGVH by injecting bm12 splenocytes into TRAF1KO recipient mice. TRAF1-deficient KRN/I-Ag7 mice spontaneously developed severe, progressive arthritis, comparable to that seen in TRAF1-intact KRN/I-Ag7 mice. However, the anti-GPI antibody titer was significantly lower in the former group. Interestingly, the TRAF1KO mice that had background levels of anti-GPI antibodies still showed severe arthritis, although with a brief delay compared to TRAF1 sufficient mice. In addition, TRAF1KO mice were fully susceptible to passive, serum transfer experiments. In another model of autoimmunity, TRAF1KO had no effect on cGVH autoantibodies production; nor was the response to an exogenous antigen impaired. The pathogenesis of spontaneous KRN/I-Ag7 arthritis can largely proceed by TRAF1-independent pathways. The production of anti-GPI autoantibody, but not other autoantibody or antibody responses, was markedly impaired by TRAF1 deficiency. The spontaneous arthritis model in KRN mice appears to be much less antibody dependent than previously believed.
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