Kono Dwight H, Theofilopoulos Argyrios N
Department of Immunology/IMM3, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA, 92037, USA.
Springer Semin Immunopathol. 2006 Oct;28(2):83-96. doi: 10.1007/s00281-006-0030-7. Epub 2006 Sep 14.
Genetic studies in spontaneous, induced, and gene-manipulated mouse models of SLE have provided significant insights into the potential number and diversity of genes that can promote, resist, and modify lupus susceptibility. Novel genes and mechanisms of disease pathogenesis have also been identified. Importantly, mouse models have provided an initial view of the genomic landscape of lupus-affecting genes, and have documented the complexities of verifying and determining the role of specific candidate loci and genes. Mouse models of lupus should continue to serve as a vital approach to defining the genetics of SLE.
在系统性红斑狼疮（SLE）的自发、诱导和基因操纵小鼠模型中进行的遗传学研究，为可能促进、抵抗和改变狼疮易感性的基因数量和多样性提供了重要见解。还发现了疾病发病机制的新基因和新机制。重要的是，小鼠模型提供了影响狼疮的基因的基因组格局的初步观点，并记录了验证和确定特定候选基因座和基因作用的复杂性。狼疮小鼠模型应继续作为确定SLE遗传学的重要方法。
