Flow cytometric analysis of antigen-specific B and T cell responses to heterologous immunization reveals intact dendritic cell function, but selective defects in germinal center formation, in mice with concurrent malaria.

CD169⁺ macrophages in the bone marrow of malaria-infected mice uptake infected red blood cells, and establish a functional interaction that is required to activate plasmacytoid dendritic cells to secrete type I interferon and leave the bone marrow.

Host cell acid ceramidase activity contributes to the regulation of erythrocyte maturation and thereby affects the frequency of target cells for rodent Plasmodium yoelii parasites.

Ecological and evolutionary perspectives are critical to understand, predict, prevent, and treat malaria parasites that may spread to humans from our close primate relatives.

Comparative transcriptomics of whole blood can be used to evaluate the systemic host response and its concordance between human and mouse malaria and aid the selection of appropriate models for translational malaria research.

With a data-driven mathematical modelling approach, within-host ecological information alone can provide clues on the mechanistic basis of diverse malaria infection outcomes.

Malaria remodels the spleen to imprint tolerance and reduce pathology in subsequent infections.

A comprehensive structural analysis of inhibitory murine antibody 3D11 binding to Plasmodium berghei circumsporozoite protein reveals common mechanisms of antibody evolution in mammals against Plasmodium parasites.

Illustrating the impact of host metabolism on infection outcome, loss of the aryl hydrocarbon receptor in radioresistant cells leads to heme-mediated kidney toxicity during malaria.