Interferon-γ signal drives differentiation of T-bet<sup>hi</sup> atypical memory B cells into plasma cells following Plasmodium vivax infection
1
Issued Date
2022-12-01
Resource Type
eISSN
20452322
Scopus ID
2-s2.0-85126746341
Pubmed ID
35318412
Journal Title
Scientific Reports
Volume
12
Issue
1
Rights Holder(s)
SCOPUS
Bibliographic Citation
Scientific Reports Vol.12 No.1 (2022)
Suggested Citation
Kochayoo P., Thawornpan P., Wangriatisak K., Changrob S., Leepiyasakulchai C., Khowawisetsut L., Adams J.H., Chootong P. Interferon-γ signal drives differentiation of T-bet<sup>hi</sup> atypical memory B cells into plasma cells following Plasmodium vivax infection. Scientific Reports Vol.12 No.1 (2022). doi:10.1038/s41598-022-08976-6 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/86437
Title
Interferon-γ signal drives differentiation of T-bet<sup>hi</sup> atypical memory B cells into plasma cells following Plasmodium vivax infection
Author's Affiliation
Other Contributor(s)
Abstract
For development of a long-lasting protective malaria vaccine, it is crucial to understand whether Plasmodium-induced memory B cells (MBCs) or plasma cells develop and stably contribute to protective immunity, or on the contrary the parasite suppresses antibody responses by inducing MBC dysfunction. The expansion of T-bethi atypical MBCs is described in chronic Plasmodium falciparum-exposed individuals. However, it remains unclear whether accumulation of T-bethi atypical MBCs is indicative of a protective role or rather an impaired function of the immune system in malaria. Here, the phenotypic and functional features of T-bethi atypical MBCs were studied in P. vivax patients living in an area of low malaria transmission. During P. vivax infection, the patients produced a twofold higher frequency of T-bethi atypical MBCs compared to malaria non-exposed individuals. This distinct atypical MBC subset had a switched IgG phenotype with overexpression of activation markers and FcRL5, and decreased Syk phosphorylation upon BCR stimulation. Post-infection, expansion of T-bethi IgG+ atypical MBCs was maintained for at least 3 months. Further studies of the contribution of T-bethi atypical MBC function to humoral immunity showed that synergizing IFN-γ with TLR7/8 and IL-21 signals was required for their differentiation into plasma cells and antibody secretion.