The role of the inflammatory cytokine MIF has been implicated on inflammatory immune response during toxoplasmosis, where an inflammatory immune response, initiated by high levels of the cytokine IL-12 produced by mature DCs, is required to control the infection. Previously we have demonstrated that MIF knockout mice are highly susceptible to T. gondii infection, due to low IL-12 levels in serum, which in turn, may be associated with a deficient maturation of DCs in the acute infection by this parasite. Therefore, the aim of this study was to determine the role of MIF on the maturation of conventional DCs during the acute infection by T. gondii. To accomplish this goal, through flow cytometry, we analyzed the maturation (IL-12 intracellular and CD40 expression) of different conventional DCs subpopulations (CD11c+ CD11b-high, CD11c+ CD11b-low and CD11c+ CD8α+) in spleens from infected and non-infected MIFKO and WT mice 24 or 48h after ip infection with T. gondii. The results demonstrated that conventional DCs subpopulations CD11c+ CD11b-high and CD11c+ CD8+α from MIF KO mice showed a lower percentage of cells producing IL-12 and reduced expression of CD40, respectively, compared to WT conventional DCs. These evidences suggest that MIF could modulate the maturation of certain subpopulations of conventional DCs during acute T. gondii.
- Copyright © 2013 by The American Association of Immunologists, Inc.