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Hopp, Christine S; Sekar, Padmapriya; Diouf, Ababacar; Miura, Kazutoyo; Boswell, Kristin; Skinner, Jeff; Tipton, Christopher M; Peterson, Mary E; Chambers, Michael J; Andrews, Sarah; Lu, Jinghua; Tan, Joshua; Li, Shanping; Doumbo, Safiatou; Kayentao, Kassoum; Ongoiba, Aissata; Traore, Boubacar; Portugal, Silvia; Sun, Peter D; Long, Carole; Koup, Richard A; Long, Eric O; McDermott, Adrian B; Crompton, Peter D
The Journal of experimental medicine, 04/2021, Letnik: 218, Številka: 4Journal Article
IgG antibodies play a role in malaria immunity, but whether and how IgM protects from malaria and the biology of Plasmodium falciparum (Pf)-specific IgM B cells is unclear. In a Mali cohort spanning infants to adults, we conducted longitudinal analyses of Pf- and influenza-specific B cells. We found that Pf-specific memory B cells (MBCs) are disproportionally IgM+ and only gradually shift to IgG+ with age, in contrast to influenza-specific MBCs that are predominantly IgG+ from infancy to adulthood. B cell receptor analysis showed Pf-specific IgM MBCs are somatically hypermutated at levels comparable to influenza-specific IgG B cells. During acute malaria, Pf-specific IgM B cells expand and upregulate activation/costimulatory markers. Finally, plasma IgM was comparable to IgG in inhibiting Pf growth and enhancing phagocytosis of Pf by monocytes in vitro. Thus, somatically hypermutated Pf-specific IgM MBCs dominate in children, expand and activate during malaria, and produce IgM that inhibits Pf through neutralization and opsonic phagocytosis.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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