<i>Plasmodium</i>-specific atypical memory B cells are not part of the long-lived memory response

Pérez‐Mazliah, Damián; Pj, Gardner; Schweighoffer, Edina; McLaughlin, Sarah; Hosking, Caroline; Tumwine, Irene; Davis, Ronald L.; Aj, Potocnik; Tybulewicz,; Langhorne, Jean

doi:10.1101/350819

Cited by 4 publications

(4 citation statements)

References 72 publications

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“…80 A recent study by P erez-Mazliah et al analyzed the MSP1-specific memory B-cell compartment following Plasmodium infection and found that atypical memory B cells were short-lived and had activated B-cell and plasmablast gene signatures. 84 Mouse studies have not resolved these issues, as age-associated memory B cells can readily respond to Toll-like receptor stimulation, 85,86 whereas in some studies, human atypical memory B cells do not. 87 Clearly, additional studies must be performed to explain the differences in these sets of studies.…”

Section: Atypical Memory B Cells In Plasmodium-infected Individualsmentioning

confidence: 99%

Basics of memory B‐cell responses: lessons from and for the real world

Wong

Bhattacharya

2018

Immunology

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Summary The production of pathogen‐specific B cells and antibodies underlies protective immunity elicited by most vaccines and many infections. Humoral immunity follows a regulated process by which high‐affinity antibody‐secreting plasma cells and memory B cells are generated. Yet for certain pathogens, protective immunity is inefficiently generated and/or maintained. For example, Dengue virus infections lead to lasting immunity against re‐infection by the same serotype. However, if infected with a different Dengue serotype, the individual is predisposed to more severe disease than if he/she was completely naive. As another example, both natural infections with or vaccination against malaria do not necessarily lead to lasting immunity, as the same individual can be re‐infected many times over the course of a lifetime. In this review, we discuss how these real‐world problems can both instruct and be informed by recent basic studies using model organisms and antigens. An emphasis is placed on protective epitopes and functional distinctions between memory B‐cell subsets in both mice and humans. Using flavivirus and Plasmodium infections as examples, we also speculate on the differences between ineffective B‐cell responses that actually occur in the real world, and perfect‐world responses that would generate lasting immunity.

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Section: Atypical Memory B Cells In Plasmodium-infected Individualsmentioning

confidence: 99%

Basics of memory B‐cell responses: lessons from and for the real world

Wong

Bhattacharya

2018

Immunology

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“…Surprisingly, we did not detect enrichment for memory B and T cells, specifically, which would have suggested anti-malarial immune memory development during one transmission season. This could partially be due to the limited resolution of our gene expression deconvolution technique in distinguishing precisely between memory and naïve lymphocyte populations, the atypical, exhausted phenotype of memory lymphocytes that develop after malaria infection and have unique gene expression profiles 17,18,20,56,57 , or a true defect in memory cell generation over few infections. Future work with more high-resolution techniques such as flow cytometry will be necessary to confirm our results and disentangle these possibilities.…”

Section: Discussionmentioning

confidence: 99%

Immune gene expression changes more during a malaria transmission season than between consecutive seasons.

Tebben,

Yirampo,

Coulibaly

et al. 2024

Preprint

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Plasmodium parasites caused over 600,000 deaths in 2022. In Mali, P. falciparum is responsible for the majority of malaria cases and deaths and is transmitted seasonally. Anti-malarial immunity develops slowly over repeated exposures to P. falciparum but some aspects of this immunity (e.g., antibody titers) wane during the non-transmission, dry season. Here, we sequenced RNA from 33 pediatric blood samples collected during P. falciparum infections at the beginning or end of a transmission season and characterized the host and parasite gene expression profiles of paired, consecutive infections. Our analyses showed that human gene expression changes more over the course of one transmission season than it does between seasons, with signatures consistent with the partial development of adaptive immunity during one transmission season, contrasting with the stability in gene expression during the dry season. By contrast, P. falciparum gene expression did not seem to vary significantly and remained stable both across and between seasons. Overall, our results provide novel insights into the dynamics of anti-malarial immunity development over short timeframes.

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“…To facilitate the identification of PrePC and PreMem populations we included CITEseq 31 Abs specific for the PrePC marker CD69 and CD38 which is upregulated on PreMem cells 15,32,33 . We also included antibodies specific for CD11c and CXCR3 to distinguish atypical B cells from conventional MBCs 34,35 .…”

Section: Because We Can See Stereotypic Selective Sweeps Occurring Am...mentioning

confidence: 99%

Plasma cells are formed in waning germinal centers via an affinity-independent process

Sutton

Parker

Lofgren

et al. 2023

Preprint

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Long-lived plasma cells (PCs) secrete antibodies that can provide sustained immunity against infection. It has been proposed that high affinity cells are preferentially selected into this compartment, potentiating the immune response. Here we used single cell RNA-seq to track the development of Ighg2A10 cells, specific for the Plasmodium falciparum circumsporozoite protein (PfCSP) within the germinal center (GC). We identified cells differentiating into memory B cells (MBC) or PCs and estimated their affinity by V(D)J sequencing. While pre-memory cells were of lower affinity than GC B cells generally, the affinity of pre-PC cells was indistinguishable. Rather, a larger proportion of cells differentiated into PCs in waning GCs. These later emigrants replaced early arrivals in the bone marrow allowing the development of a high affinity PC compartment.

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Plasmodium-specific atypical memory B cells are not part of the long-lived memory response

Cited by 4 publications

References 72 publications

Basics of memory B‐cell responses: lessons from and for the real world

Basics of memory B‐cell responses: lessons from and for the real world

Immune gene expression changes more during a malaria transmission season than between consecutive seasons.

Plasma cells are formed in waning germinal centers via an affinity-independent process

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