A novel mouse model of immunization against Plasmodium chabaudi involving infectious mosquito bites and drug-treatment elicits protection against blood-stage malaria parasites, and shows that protection is not necessarily life cycle stage-specific.

Plasmodium-specific atypical memory B cells generated to naturally (mosquito) transmitted rodent malaria infection are short-lived activated B cells, and do not prevent resolution of infection or generation of long-lived memory.

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.

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.

Plasmodium falciparum kelch13 mutations that cause artemisinin resistant malaria in Southeast Asia show markedly different patterns of evolutionary selection in Africa.

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.

The cytotoxicity exerted by CD8⁺ T cells against parasitized erythroblasts helps to protect against blood-stage malaria by making parasitized cells susceptible to phagocytosis.

Malaria transmission between human and mosquito depends on the number of male and female gametocytes in the blood.