Disease-associated qualitative and quantitative trait loci in proteoglycan-induced arthritis and collagen-induced arthritis.
作者： VA Adarichev , AB Nesterovitch , JJ Jacobs , TT Glant , S Szanto
DOI: 10.1097/00000441-200404000-00004
关键词: Arthritis 、 Rheumatoid arthritis 、 Immunopathology 、 Chromosome 17 (human) 、 Autoimmune disease 、 Major histocompatibility complex 、 Cytokine 、 Medicine 、 Immunology 、 Quantitative trait locus
摘要: ABSTRACT Two autoimmune murine models—proteoglycan (aggrecan)-induced arthritis (PGIA) and collagen-induced (CIA)—were developed in parent strains, F1 F2 hybrids of major histocompatibility complex (MHC)–matched (H-2 d ) BALB/c × DBA/2 MHC-unmatched /H-2 q DBA/1 intercrosses. The goal this comparative study was to identify disease (model)-specific (PGIA or CIA) shared clinical immunologic loci 2 types genetic Qualitative (binary/susceptibility) quantitative (severity onset) trait were separated analyzed independently together with various pathophysiologic/immunologic traits, such as antigen-specific T- B-cell responses cytokine production. locus (QTL) the MHC on chromosome 17, which especially dominant CIA. In addition, chromosomes 3, 5, 10, contained both models, a total 8 QTLs (clinical traits traits) colocalized PGIA
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