Huang, Yu-Min and Adikari, Sanjaya Bandara and Båve, Ullvi and Sanna, Alessandra and Alm, Gunnar (2004) Multiple sclerosis: IFN-β induces CD123+BDCA2– dendritic cells that produce IL-6 and IL-10 and have no enhanced type I interferon production. Scandinavian Journal of Immunology, Vol. 59 (6), p. 611-612. eISSN 1365-3083. Article.
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IFN-β, an approved drug for multiple sclerosis (MS), acts on dendritic cell (DC) by suppressing their production of IL-12p40 and increasing IL-10. This results in Th2-biased immune responses. The nature of IFN-β-modulated DC remains elusive. Previously, we observed that IFN-β dose dependently induces expression of CD123, i.e. a classical marker for plasmacytoid DC, on human blood monocyte-derived myeloid DC. Such IFN-β-modulated DC produce predominantly IL-10 but are IL-12 deficient, with potent Th2 promotion. In the present study, we further characterize IFN-β-modulated DC by using recently identified blood DC antigens (BDCA) and investigate their ability to produce Type I IFN in response to virus stimulation. We show that IFN-β induces development of CD123+ DC from human blood monocytes, which coexpress BDCA4+ but are negative for BDCA2–, a specific marker for plasmacytoid DC. Such IFN-β-modulated DC produce large amounts of IL-6 and IL-10, but no IL-12p40 and have no enhanced IFN-β and IFN-β production. The findings indicate that IFN-β-modulated DC represent a myeloid DC subset with diminished CD11c, BDCA-1 and CD1a expression, having potent Th2-promoting function but lacking antiviral capacity.
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