They also demonstrated that biopsy specimens from IgAN patients were positively stained by antibody against the secretory component of
PIGR. However, it is stated that these genetic associations had not generally been observed in any other population therefore, could not be proved to be involved in IgA nephropathy causation or progression (Maxwell and Wang, 2006).
Polymeric Ig receptor (
pIgR) present on mucosal epithelial cells can bind to dimeric IgA and pentameric IgM.
S-IgA results from transcytosis of pIgA across the epithelium through binding to the
pIgR. S-IgA is released from the
pIgR by cleavage of the receptor, resulting in pIgA covalently associated with a substantial part of the
pIgR, i.e., the secretory component (22).
Finally, expression of the
pIgR and transcytosis of IgA dimers across IECs are impaired in the absence of MyD88 signaling [77].
According to previously published techniques [33, 34], we obtained the full-length pIgR gene and pcDNA4/His A-pIgR [33].
The heavy and light chains produced in plasma cells were assembled into IgA, which is on association with polymeric immunoglobulin receptor (pIgR) during transcytosing across the basolateral epithelial cells lining on the mucosa.
All these different forms are mainly found in the circulation, while secretory IgA (sIgA) is only found at mucosal surfaces and is generated by the binding of dimeric IgA via the J-chain to the polymeric immunoglobulin receptor (
pIgR) at the basolateral side of the epithelium which is subsequently transported to the luminal side (Figures 1(d) and 1(e)).