Dendritic cells (DCs) are antigen-presenting cells specialized in priming adaptive immune responses. However, DC population is not homogeneous. They are classified into different subsets. Recently, new subsets and new differentiation pathways have been characterized. However, the heterogeneity of DCs is not yet completely understood in inflammatory diseases, such as malaria. We studied malaria caused by experimental infection of mice with Plasmodium yoelii. Malaria is a complex parasitic disease, in which the blood stage represents the clinically relevant phase characterized by cyclical invasion, intracellular replication, and egress of parasites within erythrocytes, leading to hemolysis, systemic inflammation, immune modulation, and the manifestation of symptoms such as fever, anemia, and, in severe cases, multi-organ dysfunction. Here, we investigated the diversity of DCs during experimental infection of mice with Plasmodium, with a particular focus on how systemic inflammation induced by the blood-stage of the infection reshapes the splenic DC compartment. We analyzed DCs using flow cytometry to characterize phenotypic and quantitative changes across DC subsets, including conventional type 1 DCs (cDC1), conventional type 2 DCs (cDC2), plasmacytoid DCs (pDCs), and transitional DCs (tDCs). Our results revealed robust changes in the DC compartment over the course of infection, with cDC1 markedly decreasing during early stages and re-emerging by day 20 post-infection. In contrast to previous reports, pDCs remained relatively stable throughout the infection until day 15. Notably, we also observed a significant expansion of CD11c-expressing B cells, which may have confounded pDC identification and contributed to potential misinterpretation of subset dynamics in the past. cDC2s and tDCs appear stable over the course of infection, although their absolute numbers increase in parallel with the development of splenomegaly. Overall, these findings indicate that Plasmodium yoelii. infection reshapes the DC compartment, highlighting the importance of carefully resolving DC subset dynamics to avoid misinterpretation driven by infection-induced cellular changes.