ArticleBMC microbiology2026
Malaria exposure history shapes PD-1 expression across human B-cell subsets during acute Plasmodium falciparum infection.
Article in BMC microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundRepeated malaria exposure shapes humoral immunity in endemic regions. Programmed cell death protein 1 (PD-1) is an inhibitory immune receptor involved in immune regulation during infection, but its expression across human B-cell subsets during acute malaria, and its relationship to exposure history and antigen specificity, remain poorly defined.
methodsPD-1 expression and circulating B-cell subsets were analyzed by flow cytometry in 64 individuals from Uganda and Sweden with different malaria exposure backgrounds, including individuals with acute malaria and healthy controls. PD-1 expression was assessed across major B-cell subsets and compared between P. falciparum-binding and non-binding B cells. Associations with parasitemia and inflammatory markers were also examined.
resultsPD-1 expression was higher across both naïve and memory B-cell subsets during acute malaria in Ugandan individuals with ongoing malaria exposure compared with individuals with imported malaria diagnosed in Sweden. Within memory B-cell populations, PD-1 frequencies were highest on non-class-switched (IgD⁺ and IgM⁺) subsets and on P. falciparum-binding B cells. No differences in PD-1 expression were observed between paired acute and convalescent samples. Associations between PD-1 expression, parasitemia, and inflammatory markers were limited and subset-specific.
conclusionsPD-1 expression on B cells during malaria differed according to exposure history and B-cell differentiation state. Broad PD-1 induction during acute malaria was observed only in individuals living in a malaria-endemic setting, and PD-1 expression was enriched among P. falciparum-binding B cells. Together, these findings support a potential role for checkpoint pathways in humoral immune regulation during repeated malaria infections.
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