Science alert
Uteroglobin deficient mice
a novel animal model for IgA
nephropathy?
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IgA nephropathy (IgAN) is the commonest form of glomerulonephritis worldwide. It is characterised by recurrent haematuria, proteinuria, and mesangial deposits of polymeric IgA1.1 Despite extensive research its aetiology remains elusive. This arises in part from the absence of good animal models because of the significant differences between the IgA immune system in humans and animals. The structure of human IgA1 has no parallel and IgA clearance mechanisms, systemic and mucosal compartmentalisation, and handling differ across the species. Animal models have provided useful information on the role of antigen-antibody complex associated nephropathies and the progression of immune mediated glomerular damage. The pathogenesis of human IgAN however is more complex than that involved in these models. Therefore, although animal models have been informative about events after IgA deposition has occurred, lessons about the prime mechanism of mesangial IgA deposition have been largely inferred from human studies.2
Uteroglobin knockout mice represent an
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