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• W2899390811 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." @default.
• W2899390811 created "2018-11-09" @default.
• W2899390811 creator A5012147802 @default.
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• W2899390811 creator A5083916576 @default.
• W2899390811 creator A5086765457 @default.
• W2899390811 date "2018-11-02" @default.
• W2899390811 modified "2023-09-26" @default.
• W2899390811 title "Plasmodium-specific atypical memory B cells are short-lived activated B cells" @default.
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• W2899390811 doi "https://doi.org/10.7554/elife.39800" @default.
• W2899390811 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6242553" @default.
• W2899390811 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30387712" @default.
• W2899390811 hasPublicationYear "2018" @default.
• W2899390811 type Work @default.
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• W2899390811 citedByCount "42" @default.

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