| First Author | Pérez-Mazliah D | Year | 2018 |
| Journal | Elife | Volume | 7 |
| PubMed ID | 30387712 | Mgi Jnum | J:286195 |
| Mgi Id | MGI:6402359 | Doi | 10.7554/eLife.39800 |
| Citation | Pérez-Mazliah D, et al. (2018) Plasmodium-specific atypical memory B cells are short-lived activated B cells. Elife Nov 2(7):e39800 |
| abstractText | 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. |
