ArticleCell reports2025
Systemic 4-1BB stimulation augments extrafollicular memory B cell formation and recall responses during Plasmodium infection.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
12 authors.
Funding
Abstract
T-dependent germinal center (GC) output, comprising plasma cells and memory B cells (MBCs), is crucial for clearance of Plasmodium infection and protection against reinfection. In this study, we examine the effect of an agonistic antibody targeting 4-1BB (CD137) during experimental malaria. We show that exogenous 4-1BB stimulation, despite delaying the effector GC response, surprisingly enhances humoral memory recall and protection from reinfection. Single-cell RNA and assay for transposase-accessible chromatin (ATAC) sequencing of MBCs from mice receiving 4-1BB stimulation reveal populations with distinct transcriptional signatures and a chromatin landscape indicative of superior recall and proliferative potential. Importantly, our results indicate that the effects of 4-1BB stimulation are dependent on interleukin (IL)-9R signaling in B cells but independent of parasite load during primary infection. Our study proposes an immunomodulatory approach to enhance the quality of the MBC pool, providing superior protection during infection and vaccination, particularly in the context of malaria.
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