Journal of Neuroimmunology, Vol. 133 (1-2) (2002) pp. 60-71
Jean Maguire van Seventer a , Taro Nagai a,b and Gijs A. van Seventer a
a Department of Environmental Health, Boston University School of Public Health, 715 Albany Street, Talbot 2E Boston, MA 02118, USA
b Tsukiyono Hospital, Gunma, Japan
Interferon-b is thought to provide clinical improvement to multiple sclerosis (MS) patients, in part, through its ability to suppress the generation of IL-12-dependent autoimmune T helper type 1 (Th1) cells by monocyte-derived dendritic cells (DC).
We now describe how pre-incubation with 1000 U/ml of IFN-b differentially regulates expression of multiple IL-12 family members in activated, immature human DC, inhibiting CD40/IFN-g-induced p35 and p40 message levels, while enhancing p19 and Epstein-Barr virus-induced gene 3 (EBI3) levels.
IFN-b-mediated inhibition of p40 mRNA and augmentation of p19 mRNA both require de novo protein synthesis.
These findings indicate that IFN-b will be found to have contrasting effects on DC secretion of the various IL-12 family homo- and heterodimers.
© 2002 Elsevier Science B.V.