Edinburgh Research Explorer

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

Research output: Contribution to journalArticle

  • D Pérez-Mazliah
  • Peter J Gardner
  • Edina Schweighoffer
  • Sarah McLaughlin
  • Caroline Hosking
  • Irene Tumwine
  • Randall S Davis
  • Alexandre Potocnik
  • Victor LJ Tybulewicz
  • Jean Langhorne

Related Edinburgh Organisations

Open Access permissions

Open

Documents

  • Download as Adobe PDF

    Final published version, 3 MB, PDF-document

    Licence: Creative Commons: Attribution (CC-BY)

Original languageEnglish
Article numbere39800
Number of pages28
JournaleLIFE
DOIs
Publication statusPublished - 2 Nov 2018

Abstract

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.

Download statistics

No data available

ID: 86156951