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Localization and Regulation of Polymeric Ig Receptor in Healthy and Diseased Human Kidney

Journal article
Authors K. M. Krawczyk
H. Nilsson
Jenny Nyström
D. Lindgren
K. Leandersson
K. Sward
M. E. Johansson
Published in American Journal of Pathology
Volume 189
Issue 10
Pages 1933-1944
ISSN 0002-9440
Publication year 2019
Published at Institute of Neuroscience and Physiology
Pages 1933-1944
Language en
Keywords secretory immunoglobulin-a, minimal change disease, intracellular, neutralization, immune-responses, epithelial-cells, virus, nephropathy, expression, component, system, Pathology
Subject categories Pathology, Internal medicine


The polymeric Ig receptor (PIgR) constitutes an important part of the immune system by mediating transcytosis of dimeric IgA into mucosal fluids. Although well studied in organs such as the intestine, the regulation and localization of PIgR in human kidney are incompletely characterized. Herein, using immunohistochemistry, we show that in healthy human kidneys, PIgR is expressed by the progenitor-like tubular scattered cells of the proximal tubules and by parietal epithelial cells of glomeruli. We further show that proximal tubular expression of PIgR becomes widespread during kidney disease, correlating to elevated levels of urinary secretory IgA. Urinary secretory IgA levels also correlated to the degree of tubular fibrosis, plasma creatinine, and urea levels. In addition, primary tubular cells were cultured to study the function and regulation of PIgR in vitro. Cellular PIgR expression was induced by conditioned medium from activated human leukocytes, as well as by inflammatory cytokines, whereas transforming growth factor-beta 1 caused decreased expression. Furthermore, interferon-gamma increased the transcytosis of dimeric IgA in cultured tubular cells. Finally, a correlation study of mRNA data from the Genotype-Tissue Expression portal indicated that PIGR mRNA expression in kidney correlates to the expression of TNFSF13, a cytokine involved in plasma cell class switching to IgA. These results indicate that PIgR induction is an integral part of the injury phenotype of renal tubular cells. RAMOWSKY CR, 1986, AMERICAN JOURNAL OF PATHOLOGY, V125, P571

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