B cell and plasma cell responses take place in lymphoid organs, but because of the inaccessibility of these organs, analyses of human responses are largely performed using peripheral blood mononuclear cells (PBMC).
Protection against malaria often decays in the absence of infection, suggesting that protective immunological memory depends on stimulation.
Here, we investigate as to whether this conversion coincides with permanent changes of hepatic gene expression profiles. Female mice aged 10–12 weeks were treated with testosterone for 3 weeks; then, testosterone treatment was discontinued for 12 weeks before challenging with 106 P. chabaudi-infected erythrocytes.
Collectively, these data indicate that the suppression of acute P. chabaudi infection by CMI is T cell dependent, is independent of NK cells, and may be attributed to the deficient IFN response seen early in T-cell-depleted mice.
Here we show that after infection of mice with Plasmodium chabaudi, a c-Kithi progenitor subset positive for interleukin 7 receptor-α (IL-7Rα) emerged that had both lymphoid and myeloid potential in vitro.
Does specific immunity, innate immunity or resource (red blood cell) limitation control the first peak of the blood-stage parasite in acute rodent malaria infections?
Deletion of the taurine transporter gene (taut) results in lowered levels of taurine, the most abundant amino acid in mammals. Here, we show that taut–/– mice have lost their ability to self-heal blood-stage infections with Plasmodium chabaudi malaria.
CB6F1 mice infected with the nonlethal Plasmodium chabaudi chabaudi AS suffer parasitaemia levels up to 40% (full parasitaemia, FP) and develop both homologous and heterologous (against the lethal Plasmodium yoelii 17XL) protective immunity.
The cellular mechanisms underlying B cell and antibody responses are difficult to study in human infections; therefore, we have investigated the kinetics, duration and characteristics of the Plasmodium-specific memory B cell response in an infection of P. chabaudi in mice.
This study aimed to investigate the development of memory responses in susceptible A/J and resistant C57BL/6 mice which differ in the degree of susceptibility to clinical malaria following P. chabaudi AS infection.