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RelB mediates TNF-induced up-regulation of polymeric Ig receptor.

Vaccine Weekly

| October 06, 2004 | COPYRIGHT 2004 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2004 OCT 6 - (NewsRx.com & NewsRx.net) -- De novo synthesized RelB mediates TNF-induced up-regulation of the human polymeric Ig receptor.

"Secretory antibodies, which operate in a principally noninflammatory fashion, constitute the first line of acquired immune defense of mucosal surfaces. Such antibodies are generated by polymeric Ig receptor (pIgR)-mediated export of dimeric IgA and pentameric IgM. TNF activates a proinflammatory gene repertoire in mucosal epithelial cells and also enhances pIgR expression," scientists writing in the Journal of Immunology report.

"In this study we show that TNF-induced up-regulation of the human pIgR critically depends on an NF-kappaB site and flanking sequences within a 204-bp region of the first intron in the pIgR gene, a region largely overlapping with a recently characterized IL-4-responsive enhancer," said Hilde Schjerven and colleagues at Rikshospitalet University Hospital. "The intronic NF-kappaB site was rapidly bound by NF-kappaB p65/p50 heterodimers present in nuclear extracts after TNF treatment of HT-29 cells, but a more delayed binding of ROB agreed better with the slow, protein synthesis-dependent, transcriptional activation of the pIgR gene."

"Overexpression of NF-kappaB p65 caused transient up-regulation of a pIgR-derived reporter gene, whereas overexpression of ...

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