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The Journal of Immunology, 2004, 173: 1849-1857.
Copyright © 2004 by The American Association of Immunologists

De Novo Synthesized RelB Mediates TNF-Induced Up-Regulation of the Human Polymeric Ig Receptor1

Hilde Schjerven2, Thien N. Tran2, Per Brandtzaeg and Finn-Eirik Johansen3

Laboratory for Immunohistochemistry and Immunopathology, Institute and Department of Pathology, Rikshospitalet University Hospital, Oslo, Norway

Secretory Abs, which operate in a principally noninflammatory fashion, constitute the first line of acquired immune defense of mucosal surfaces. Such Abs 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. In this study we show that TNF-induced up-regulation of the human pIgR critically depends on an NF-{kappa}B 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. The intronic NF-{kappa}B site was rapidly bound by NF-{kappa}B p65/p50 heterodimers present in nuclear extracts after TNF treatment of HT-29 cells, but a more delayed binding of RelB agreed better with the slow, protein synthesis-dependent, transcriptional activation of the pIgR gene. Overexpression of NF-{kappa}B p65 caused transient up-regulation of a pIgR-derived reporter gene, whereas overexpression of RelB showed a stronger and more sustained effect. Finally, we demonstrated that inhibition of endogenous RelB by RNA interference severely reduced the TNF responsiveness of our pIgR-derived reporter gene. Thus, TNF-induced signaling pathways required for up-regulated pIgR expression appear to differ from those of the proinflammatory gene repertoire.




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