Alm, Gunnar
- Department of Molecular Biosciences, Swedish University of Agricultural Sciences
Abstract
Interferon-beta (IFN-beta), an approved drug for multiple sclerosis (MS), acts on dendritic cells (DC) by suppressing IL-12p40 and increasing IL-10. This results in Th2-biased immune responses. The nature of IFN-beta-modulated DC remains elusive. Previously, we observed that IFN-beta dose dependently induces expression of CD123, i.e., a classical marker for plasmacytoid DC, on human blood monocyte-derived myeloid DC. Such IFN-beta-modulatcd DCs produce predominantly IL-10 but are IL-12 deficient, with potent Th2 promotion. In the present study, we further characterize IFN-beta-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-beta 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-modulated DC can produce IL-6 and IL-10 but not IL-12p40, and have no enhanced IFN-alpha and IFN-beta production. The findings indicate that IFN-beta-modulated DCs represent a myeloid DC subset with diminished CD11c, BDCA-1 and CD1a expression. They may promote Th2 and B cell differentiation through IL-6 and IL-10 production, and suppression of IL-12p40, but they have no enhanced antiviral capacity. (C) 2004 Elsevier B.V. All rights reserved.
Keywords
multiple sclerosis; interferon-beta; dendritic cells
Published in
Journal of Neuroimmunology
2005, volume: 158, number: 45659, pages: 204-212
Publisher: ELSEVIER SCIENCE BV
SLU Authors
UKÄ Subject classification
Immunology in the medical area
Publication identifier
- DOI: https://doi.org/10.1016/j.jneuroim.2004.08.014
Permanent link to this page (URI)
https://res.slu.se/id/publ/5580