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.
The association of atypical memory B-cells and autoimmune antibodies (anti-phosphatidylserine) with hemoglobin levels in malaria patients uncovers a novel mechanism for the human malaria-induced anemia previously identified in mice.
Atypical memory B cells (MBCs) appear to differentiate from classical MBCs during chronic exposure to the malaria parasite Plasmodium falciparum, and may interfere with the acquisition of immunity to the disease.
Epithelial cells coordinate integrin signaling with protrusion via a two-protein module, with one protein defining localization and downstream signaling, the other serving as a phosphorylation switch and providing negative feedback.
Experiments in a mouse model for Alzheimer’s disease using germ-free and conventionally housed animals reveal that microbiota-derived short-chain fatty acids promote the deposition of cerebral Aβ plaques.