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Systemic lupus erythematosus ? recent clues from congenic strains

100%

Henry T. , Mohan C.

Archivum Immunologiae et Therapiae Experimentalis

2005

tom 53

nr 3

207-212

Systemic lupus erythematosus is a polycongenic autoimmune disease characterized by the production of antinuclear antibodies that lead to subsequent end organ damage. The study of lupus is complicated by its polycongenic origin, contributions from hormones and the environment, epistasis among susceptibility loci, suppressive modifiers, and the fact that a single susceptibility locus may encompass multiple susceptibility genes. Murine models that develop lupus spontaneously have greatly contributed to our understanding of this disease. In particular, the advent of ?congenic strains' has greatly simplified the study of this complex autoimmune disease. Thus, congenic strains bearing NZB/NZW/NZM2410, BXSB, and MRL lupus susceptibility loci are steadily replacing the traditionally studied murine lupus models as the models of choice for research. This review summarizes how researchers have used congenic strains over the past few years to dissect out and reconstruct the individual elements contributing to lupus pathogenesis.

Experimental anti-GBM nephritis as an analytical tool for studying spontaneous lupus nephritis

80%

Du Y. , Fu Y. , Mohan C.

Archivum Immunologiae et Therapiae Experimentalis

2008

tom 56

nr 1

31-40

Systemic lupus erythematosus (SLE) is an autoimmune disease that results in immune-mediated damage to multiple organs. Among these, kidney involvement is the most common and fatal. Spontaneous lupus nephritis (SLN) in mouse models has provided valuable insights into the underlying mechanisms of human lupus nephritis. However, SLN in mouse models takes 6?12 months to manifest; hence there is clearly the need for a mouse model that can be used to unveil the pathogenic processes that lead to immune nephritis over a shorter time frame. In this article more than 25 different molecules are reviewed that have been studied both in the anti-glomeruali basement membrane (anti-GBM) model and in SLN and it was found that these molecules influence both diseases in a parallel fashion, suggesting that the two disease settings share common molecular mechanisms. Based on these observations, the authors believe the experimental anti-GBM disease model might be one of the best tools currently available for uncovering the downstream molecular mechanisms leading to SLN.