Plasmodium-specific atypical memory B cells are short-lived activated B cells

Academic Article

Abstract

  • © Pérez-Mazliah et al. A 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, Plasmodium chabaudi. In combination with a mosquito-initiated P. chabaudi infection, we show that Plasmodium-specific atypical memory B cells are short-lived and disappear upon natural resolution of chronic infection. These cells show features of activation, proliferation, DNA replication, and plasmablasts. Our data demonstrate that Plasmodium-specific atypical memory B cells are not a subset of long-lived memory B cells, but rather short-lived activated cells, and part of a physiologic ongoing B-cell response.
  • Published In

  • eLife  Journal
  • Digital Object Identifier (doi)

    Author List

  • Pérez-Mazliah D; Gardner PJ; Schweighoffer E; McLaughlin S; Hosking C; Tumwine I; Davis RS; Potocnik AJ; Tybulewicz VLJ; Langhorne J
  • Volume

  • 7