These studies demonstrate exacerbated neuroinflammation concurrent with development of behavioural symptoms in P. chabaudi infection of IL-10−/− animals.
Protective vaccination induces self-healing of otherwise lethal blood-stage infections of Plasmodium chabaudi malaria.
Many microparasites infect new hosts with specialized life stages, requiring a subset of the parasite population to forgo proliferation and develop into transmission forms.
CD4 T cells are required to fight malaria infection by promoting both phagocytic activity and B cell responses for parasite clearance.
Acute lower respiratory tract infections (ALRTI) are the leading cause of global childhood mortality, with human respiratory syncytial virus (hRSV) being a major cause of viral ALRTI in young children worldwide.
Interleukin-21 signaling is important for germinal center B-cell responses, isotype switching and generation of memory B cells.
Some of the data in the article  were inadvertently mislabelled.
To follow the fate of CD8+ T cells responsive to Plasmodium berghei ANKA (PbA) infection, we generated an MHC I-restricted TCR transgenic mouse line against this pathogen.
The mechanism by which protective immunity to Plasmodium is lost in the absence of continued exposure to this parasite has yet to be fully elucidated.
It is beneficial for parasites to be in synchronization with their host's rhythm, regardless of the route of infection or the parasite stage inoculated.