Abstract
Animal models of autoimmune diseases have been instrumental in advancing our understanding of autoimmunity in humans. Collagen-induced arthritis (CIA) in mice is an autoimmune disease model of rheumatoid arthritis. Susceptibility to CIA in mice is linked to genes of the major histocompatibility complex (MHC). CD4+ T cells that express the T-cell receptor (TCR) Tcra-V11.1 and/or Tcrb-V8.2 play a key role in the pathogenesis of arthritis in the DBA/1 mouse (H2 q). We identified an inbred mouse strain, FVB/NJ (H2 q), that is resistant to arthritis induction and exhibits a genomic deletion of certain Tcrb-V gene segments. We report a novel polymerase chain reaction-based method for the rapid identification of new mouse strains that exhibit germline Tcrb-V gene deletions. We mapped for the first time both the 5′ and 3′ breakpoints of the Tcrb-V deletion in the FVB/NJ, SWR, SJL, C57L, and C57BR strains to within 1.1 kilobases. Since there is an association between a particular Tcra-V allele (Tcra-V11.1 d) and arthritis susceptibility in H2 q mouse strains, we examined the allelic polymorphisms of the Tcra-V11 gene subfamily members between the arthritis-susceptible DBA/1 mouse and the arthritis-resistant FVB/NJ mouse strain. The amino acid sequences of the Tcra-V11.1 alleles differ at two positions (codons 18 and 68). Therefore, the resistance of FVB/NJ mouse to arthritis induction may be due in part to Tcra-V11.1 coding sequence polymorphism and Tcrb-V8.2 gene segment deletion, as we have recently demonstrated in the case of SWR mouse strain.
Similar content being viewed by others
Author information
Authors and Affiliations
Additional information
Received: 12 January 1999 / Revised: 17 March 1999
Rights and permissions
About this article
Cite this article
Osman, G., Hannibal, M., Anderson, J. et al. FVB/N (H2 q) mouse is resistant to arthritis induction and exhibits a genomic deletion of T-cell receptor V beta gene segments. Immunogenetics 49, 851–859 (1999). https://doi.org/10.1007/s002510050564
Issue Date:
DOI: https://doi.org/10.1007/s002510050564