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.

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.

In an autoimmune environment B cells mature from spontaneous germinal centers into transcriptomically and phenotypically diverse memory and antibody-secreting cells but maintaining shared clonal and potential self-reactive specificities which has important implications for pathogenic cell targeted depletion.

A skewed B cell response in people living with HIV proceeds via an extrafollicular path and could result in reduced affinity B cell memory and antibody responses.

Circulating T follicular helper cells appear to be a promising biomarker candidate for monitoring vaccine efficacy in malaria vaccine trials.

A neural network model of the hippocampus exhibits a division of labor across its two main pathways during category learning, with one pathway specializing in extracting systematic category information and another in encoding arbitrary details.

Improved cell-type-specific genetic drivers for the study of learning and memory and other complex behaviors in Drosophila are provided and validated.

Androgen receptor activation modifies B cell frequencies and functionality, accompanied by weight gain in female mice exposed to human PCOS IgG, highlighting the unrecognized involvement of B cells in PCOS autoimmune comorbidities despite their absence not preventing PCOS phenotype development.

Input from the ventral hippocampus to the medial prefrontal cortex regulates social memory in wild type mice and atypically-strengthened input causes social memory dysfunction in Rett syndrome mice.