Plasmodium-specific atypical memory B cells are short-lived activated B cells.
Plasmodium-specific atypical memory B cells are short-lived activated B cells.
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DOI:
10.7554/elife.39800
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发表时间:
2018-11-02
期刊:
影响因子:
7.7
通讯作者:
Langhorne J
中科院分区:
文献类型:
--
作者:
Pérez-Mazliah D;Gardner PJ;Schweighoffer E;McLaughlin S;Hosking C;Tumwine I;Davis RS;Potocnik AJ;Tybulewicz VL;Langhorne J
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.