Abstract
Polymeric IgA (pIgA) is transcytosed by the pIgA receptor (pIgR) across mucosal epithelial cells. After transcytosis to the apical surface, the extracellular, ligand-binding portion of the pIgR is proteolytically cleaved. A missense mutation in human pIgR, A580V, is associated with IgA nephropathy and nasopharyngeal carcinoma. We report that this mutation reduces the rate of transcytosis of pIgR and pIgA, and seemingly the rate of pIgR cleavage. We propose that the defects in pIgR trafficking caused by the A580V mutation may underlie the pathogenesis of both diseases.
Highlights
The A580V human Polymeric IgA (pIgA) receptor (pIgR) polymorphism is associated with IgA nephropathy and nasopharyngeal carcinoma
We propose that the defects in pIgR trafficking caused by the A580V mutation may underlie the pathogenesis of both diseases
We determined the effect of the mutation on AP secretory component (SC) release in the presence of pIgA added to the BL medium
Summary
The A580V human pIgR polymorphism is associated with IgA nephropathy and nasopharyngeal carcinoma. A missense mutation in human pIgR, A580V, is associated with IgA nephropathy and nasopharyngeal carcinoma We report that this mutation reduces the rate of transcytosis of pIgR and pIgA, and seemingly the rate of pIgR cleavage. A missense mutation (pIgR-A580V) in the extracellular region of human pIgR is associated with increased risk of IgA nephropathy (IgAN) in Japan [4]. PIgR-A580V mutation has been associated in two studies with increased risk of nasopharyngeal carcinoma (NPC) in Thai and southern Chinese populations, where NPC is a leading form of cancer (6 – 8) This result is intriguing, because EpsteinBarr virus (EBV), the causative agent of NPC, can enter epithelial cells via binding to the pIgR of pIgA antibodies directed against EBV [9, 10]
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