Abstract
Systemic lupus erythematosus (SLE) involves multiple genes. Major genes that predispose to SLE are related to key events in pathogenesis, and may involve a variety of genes in immune system. Because of complex polygenic control and of heterogeneity of human genome, several hundred affected sibpairs are assumed to be necessary to show linkages for many of the contributing loci. In this respect, SLE-prone mouse strains are useful for the genome-wide search of SLE-susceptibility candidate genes. In the present studies, we analyzed genetic contribution to the aberrant activation of B cells using SLE-prone (NZB×NZW) F1 mouse model. Results showed that NZB type regulatory region polymorphism in FcγR IIB gene on chromosome 1 was significantly linked to hyper-IgG and high level of IgG anti-DNA antibodies. Extensive studies on murine models are expected to form the basis for identification of target genes and for clarification of the genetic mechanisms underlying SLE.
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