Rapid activation of spleen dendritic cell subsets following lymphocytic choriomeningitis virus infection of mice: analysis of the involvement of type 1 IFN

M Montoya, MJ Edwards, DM Reid… - The Journal of …, 2005 - journals.aai.org
M Montoya, MJ Edwards, DM Reid, P Borrow
The Journal of Immunology, 2005journals.aai.org
In this study, we report the dynamic changes in activation and functions that occur in spleen
dendritic cell (sDC) subsets following infection of mice with a natural murine pathogen,
lymphocytic choriomeningitis virus (LCMV). Within 24 h postinfection (pi), sDCs acquired the
ability to stimulate naive LCMV-specific CD8+ T cells ex vivo. Conventional (CD11c high
CD8+ and CD4+) sDC subsets rapidly up-regulated expression of costimulatory molecules
and began to produce proinflammatory cytokines. Their tendency to undergo apoptosis ex …
Abstract
In this study, we report the dynamic changes in activation and functions that occur in spleen dendritic cell (sDC) subsets following infection of mice with a natural murine pathogen, lymphocytic choriomeningitis virus (LCMV). Within 24 h postinfection (pi), sDCs acquired the ability to stimulate naive LCMV-specific CD8+ T cells ex vivo. Conventional (CD11c high CD8+ and CD4+) sDC subsets rapidly up-regulated expression of costimulatory molecules and began to produce proinflammatory cytokines. Their tendency to undergo apoptosis ex vivo simultaneously increased, and in vivo the number of conventional DCs in the spleen decreased markedly, dropping∼ 2-fold by day 3 pi. Conversely, the number of plasmacytoid (CD11c low B220+) DCs in the spleen increased, so that they constituted almost 40% of sDCs by day 3 pi. Type 1 IFN production was up-regulated in plasmacytoid DCs by 24 h pi. Analysis of DC activation and maturation in mice unable to respond to type 1 IFNs implicated these cytokines in driving infection-associated phenotypic activation of conventional DCs and their enhanced tendency to undergo apoptosis, but also indicated the existence of type 1 IFN-independent pathways for the functional maturation of DCs during LCMV infection.
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