Assessing the function of human UNC-93B in Toll-like receptor signaling and major histocompatibility complex II response.
Hum Immunol
; 68(11): 871-8, 2007 Nov.
Article
en En
| MEDLINE
| ID: mdl-18082565
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.
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Bases de datos:
MEDLINE
Asunto principal:
Proteínas de Transporte de Membrana
/
Transducción de Señal
/
Antígenos de Histocompatibilidad Clase II
/
Presentación de Antígeno
/
Receptores Toll-Like
/
Células Presentadoras de Antígenos
Tipo de estudio:
Prognostic_studies
Límite:
Humans
Idioma:
En
Revista:
Hum Immunol
Año:
2007
Tipo del documento:
Article
País de afiliación:
Austria