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© Research
Publication : Journal of leukocyte biology

Differential responsiveness to IFN-alpha and IFN-beta of human mature DC through modulation of IFNAR expression

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of leukocyte biology - 19 Apr 2006

Severa M, Remoli ME, Giacomini E, Ragimbeau J, Lande R, Uzé G, Pellegrini S, Coccia EM

Link to Pubmed [PMID] – 16624932

J. Leukoc. Biol. 2006 Jun;79(6):1286-94

In human monocyte-derived dendritic cells (DC), infection with Mycobacterium tuberculosis and viruses or stimulation with Toll-like receptor type 3 and 4 agonists causes the release of type I interferon (IFN). Here, we describe that the IFN-beta released upon stimulation with lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (poly I:C) is responsible for a rapid and sustained signal transducer and activator of transcription 1 and 2 activation and expression of IFN-stimulated genes, such as the transcription factor IFN regulatory factor 7 and the chemokine CXC chemokine ligand 10. The autocrine production of IFN-beta from LPS and poly I:C-matured DC (mDC) induced a temporary saturation of the response to type I IFN and a marked decline in the level of the two IFN receptor (IFNAR) subunits. It is interesting that we found that upon clearing of the released cytokines, LPS-stimulated DC reacquired full responsiveness to IFN-beta but only partial responsiveness to IFN-alpha, and their maturation process was unaffected. Monitoring of surface and total levels of the receptor subunits showed that maximal expression of IFNAR2 resumed within 24 h of clearing, and IFNAR1 expression remained low. Thus, mDC can modulate their sensitivity to two IFN subtypes through a differential regulation of the IFNAR subunits.

http://www.ncbi.nlm.nih.gov/pubmed/16624932