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.
Original language | English |
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Article number | e39800 |
Number of pages | 28 |
Journal | eLife |
Volume | 7 |
DOIs | |
Publication status | Published - 2 Nov 2018 |
Bibliographical note
© 2018, Pérez-Mazliah et al.Keywords
- Animals
- B-Lymphocyte Subsets/chemistry
- B-Lymphocytes/chemistry
- Flow Cytometry
- Gene Knock-In Techniques
- Immunoglobulin G/genetics
- Immunologic Memory
- Malaria/immunology
- Merozoite Surface Protein 1/immunology
- Mice, Inbred BALB C
- Mice, Inbred C57BL
- Plasmodium chabaudi/immunology
- Rodent Diseases/immunology