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Journals The FASEB Journal July 2009

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Increased I{kappa}B{alpha} expression is essential for the tolerogenic property of TGF-{beta}-exposed APCs

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I B is an inhibitor of the transcriptional factor NF- B, and it is an essential component of the signaling pathways that lead to expression of inflammatory molecules. These include cytokines and costimulatory molecules associated with antigen presentation in an inflammatory immune response. In this study, we report that antigen-presenting cells exposed to TGF-β induce peripheral tolerance by increasing I B expression. Exposure of antigen presenting cells (APCs) to TGF-β is known to impair their ability to secrete IL-12, and such impairment correlated with reduced NF- B activity as indicated by significantly reduced nuclear levels of p50, an essential subunit of NF- B for IL-12 transcription. Blockade of increased nuclear I B in APCs by expression of small interfering RNA molecules (siRNAs) targeting I B transcripts prevented IL-12 impairment and the decline in nuclear p50 levels. Furthermore, such I B blockade also interfered with the tolerogenic property of TGF-β- exposed APCs. However, increased expression of I B in APCs, independent of TGF-β exposure, reduced nuclear p50 levels and permitted tolerance induction by APCs. Thus, our findings attribute a direct and significant role to I B in the tolerogenic potential of APCs. Increased I B expression in APCs may therefore offer a therapeutic approach to achieve antigen-specific immunomodulation.—Ghafoori, P., Yoshimura, T., Turpie, B., Masli, S. Increased I B expression is essential for the tolerogenic property of TGF-β-exposed APCs.

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Article Details
Ghafoori, Paiman; Yoshimura, Takeru; Turpie, Bruce; Masli, Sharmila
The FASEB Journal , Volume 23 (7): 2226
Fed of American Socs for Experimental Biology – Jul 1, 2009
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