- D Pérez-Mazliah
- Peter J Gardner
- Edina Schweighoffer
- Sarah McLaughlin
- Caroline Hosking
- Irene Tumwine
- Randall S Davis
- Alexandre Potocnik
- Victor LJ Tybulewicz
- Jean Langhorne
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Final published version, 3.76 MB, PDF document
Licence: Creative Commons: Attribution (CC-BY)
Original language | English |
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Article number | e39800 |
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Number of pages | 28 |
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Journal | eLIFE |
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DOIs | |
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Publication status | Published - 2 Nov 2018 |
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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.
ID: 86156951