Krawczyk KM, Nilsson H, Nyström J, et al. - Via immunohistochemistry, researchers demonstrated that in healthy human kidneys, polymeric immunoglobulin receptor (PIgR) was expressed by the progenitor-like tubular scattered cells of the proximal tubules and by parietal epithelial cells of glomeruli and that proximal tubular expression of PIgR became widespread during kidney disease, corresponding to high levels of urinary secretory IgA as determined by ELISA. Urinary secretory IgA levels also related to the degree of tubular fibrosis, plasma creatinine, and urea levels. Moreover, primary tubular cells were cultured to examine the function and regulation of PIgR in vitro. Cellular PIgR expression was caused by conditioned medium from activated human leukocytes, as well as by inflammatory cytokines, whereas transforming growth factor-β1 led to reduced expression. Further, in cultured tubular cells, IFNγ rose the transcytosis of dimeric IgA. Lastly, an association study of mRNA data from the Genotype-Tissue Expression portal showed that PIGR mRNA expression in kidney corresponded to the expression of TNFSF13, a cytokine involved in plasma cell class switching to IgA. Hence, PIgR induction was concluded as an integral part of the injury phenotype of renal tubular cells.