Elucidation of the pathogenic mechanism of IgA nephropathy through identification and functional analysis of the receptor for the insufficient glycosylated IgA molecules

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IgA nephropathy is characterized by mesangial deposition of IgA1 and galactose-deficient IgA1 is assumed to play a pathogenic role. However, the identity of the receptor for IgA1 is still controversial. Hence, the aim of this study was to explore the receptor for galactose-deficient IgA1. Human monoclonal IgA1 was treated with exoglycosidase and FITC-conjugated galactose-deficient IgA1 was used as a probe to detect the receptor in cultured human mesangial cells. According to comprehensive gene expression analysis, we revealed that galactose-deficient IgA1-collagen complex formation would be proposed as one of the candidate mechanisms of IgA1 deposition and proliferative signal transduction via integrinα2/β1 heterodimer in human mesangial cells.