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

Jadranka Koehn, Dieter Huesken, Markus Jaritz, Antal Rot, Mauro Zurini, Anne Dwertmann, Bruce Beutler, Ulf Korthäuer

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


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 [1]. 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 TNFα 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.

Original languageEnglish (US)
Pages (from-to)871-878
Number of pages8
JournalHuman Immunology
Issue number11
StatePublished - Nov 2007


  • Adaptive immune system
  • Dendritic cells
  • Innate immunity
  • Toll-like receptors
  • siRNA

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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