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Assessing the function of human UNC-93B in Toll-like receptor signaling and major histocompatibility complex II response.

Koehn, Jadranka and Huesken, Dieter and Jaritz, Markus and Rot, Antal and Zurini, Mauro and Dwertmann, Anne and Beutler, Bruce and Korthauer, Ulf (2007) Assessing the function of human UNC-93B in Toll-like receptor signaling and major histocompatibility complex II response. Human Immunology, 68 (11). pp. 871-878. ISSN 0198-8859

Abstract

The high sequence identity observed between UNC-93B of mouse and human imply common evolutionary ancestors and a conserved function. A nonconservative point mutation in the mouse Unc93b1 gene has been associated with defective Toll-like receptor (TLR) signaling and impaired major histocompatibility complex (MHC) I and II restricted antigen responses. Like murine UNC-93B, the human homologue is predicted to form 12 transmembrane domains, and it localizes to the endoplasmic reticulum. In human beings its expression is highest in professional antigen-presenting cells such as dendritic cells and macrophages. Interestingly, UNC-93B itself is specifically induced by TLR3 signaling in monocyte-derived dendritic cells and macrophages. To study the effect of UNC-93B deficiency in TLR signaling and antigen-presentation in human beings, UNC-93B message was knocked down in monocyte-derived dendritic cells and a reduced TNFalpha production in response to TLR3 agonists was observed. In the same experiment, the achieved knockdown had no effect on an MHC II-dependent antigen response, suggesting that the reduced quantity of human UNC-93B was still capable of supporting class II antigen presentation or that UNC-93B is not required for class II antigen presentation in human antigen-presenting cells.

Item Type: Article
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Additional Information: author can archive post-print (ie final draft post-refereeing); Publisher's version/PDF cannot be used
Keywords: Dendritic cells; siRNA; Adaptive immune system; Innate immunity; Toll-like receptors
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Date Deposited: 14 Dec 2009 14:01
Last Modified: 14 Dec 2009 14:01
URI: https://oak.novartis.com/id/eprint/339

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