Malaria parasite species differ greatly in the harm they do to humans. While kills hundreds of thousands per year, kills much less often and is relatively benign. Strains of the rodent malaria parasite show phenotypic variation in virulence during infections of laboratory mice.
View Article and Find Full Text PDFA subset of atypical memory B cells accumulates in malaria and several infections, autoimmune disorders and aging in both humans and mice. It has been suggested these cells are exhausted long-lived memory B cells, and their accumulation may contribute to poor acquisition of long-lasting immunity to certain chronic infections, such as malaria and HIV. Here, we generated an immunoglobulin heavy chain knock-in mouse with a BCR that recognizes MSP1 of the rodent malaria parasite, .
View Article and Find Full Text PDFCD4 follicular helper T (Tfh) cells have been shown to be critical for the activation of germinal center (GC) B-cell responses. Similar to other infections, Plasmodium infection activates both GC as well as non-GC B cell responses. Here, we sought to explore whether Tfh cells and GC B cells are required to eliminate a Plasmodium infection.
View Article and Find Full Text PDFBackground: Parasite cytoadherence within the microvasculature of tissues and organs of infected individuals is implicated in the pathogenesis of several malaria syndromes. Multiple host receptors may mediate sequestration. The identity of the host receptor(s), or the parasite ligand(s) responsible for sequestration of Plasmodium species other than Plasmodium falciparum is largely unknown.
View Article and Find Full Text PDFMalaria is caused by parasites of the genus Plasmodium. All human-infecting Plasmodium species can establish long-lasting chronic infections, creating an infectious reservoir to sustain transmission. It is widely accepted that the maintenance of chronic infection involves evasion of adaptive immunity by antigenic variation.
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