Analysis of human B ‐cell responses following C h A d63‐ MVA MSP 1 and AMA 1 immunization and controlled malaria infection

Acquisition of non‐sterilizing natural immunity to P lasmodium falciparum malaria has been shown in low transmission areas following multiple exposures. However, conflicting data from endemic areas suggest that the parasite may interfere with the induction of effective B ‐cell responses. To date, th...

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Veröffentlicht in:Immunology 2014-04, Vol.141 (4), p.628-644
Hauptverfasser: Elias, Sean C., Choudhary, Prateek, de Cassan, Simone C., Biswas, Sumi, Collins, Katharine A., Halstead, Fenella D., Bliss, Carly M., Ewer, Katie J., Hodgson, Susanne H., Duncan, Christopher J. A., Hill, Adrian V. S., Draper, Simon J.
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container_end_page 644
container_issue 4
container_start_page 628
container_title Immunology
container_volume 141
creator Elias, Sean C.
Choudhary, Prateek
de Cassan, Simone C.
Biswas, Sumi
Collins, Katharine A.
Halstead, Fenella D.
Bliss, Carly M.
Ewer, Katie J.
Hodgson, Susanne H.
Duncan, Christopher J. A.
Hill, Adrian V. S.
Draper, Simon J.
description Acquisition of non‐sterilizing natural immunity to P lasmodium falciparum malaria has been shown in low transmission areas following multiple exposures. However, conflicting data from endemic areas suggest that the parasite may interfere with the induction of effective B ‐cell responses. To date, the impact of blood‐stage parasite exposure on antigen‐specific B cells has not been reported following controlled human malaria infection ( CHMI ). Here we analysed human B ‐cell responses in a series of P hase I/IIa clinical trials, which include CHMI , using candidate virus‐vectored vaccines encoding two blood‐stage antigens: merozoite surface protein 1 ( MSP 1) and apical membrane antigen 1 ( AMA 1). Previously vaccinated volunteers show boosting of pre‐existing antigen‐specific memory B ‐cell (m BC ) responses following CHMI . In contrast, unvaccinated malaria‐naive control volunteers developed an m BC response against MSP 1 but not AMA 1. Serum I g G correlated with the m BC response after booster vaccination but this relationship was less well maintained following CHMI . A significant reduction in peripheral MSP 1‐specific m BC was observed at the point of diagnosis of blood‐stage infection. This was coincident with a reduction in peripheral blood B ‐cell subsets expressing CXCR 3 and elevated serum levels of interferon‐ γ and CXCL 9, suggesting migration away from the periphery. These CHMI data confirm that m BC and antibody responses can be induced and boosted by blood‐stage parasite exposure, in support of epidemiological studies on low‐level parasite exposure.
doi_str_mv 10.1111/imm.12226
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Here we analysed human B ‐cell responses in a series of P hase I/IIa clinical trials, which include CHMI , using candidate virus‐vectored vaccines encoding two blood‐stage antigens: merozoite surface protein 1 ( MSP 1) and apical membrane antigen 1 ( AMA 1). Previously vaccinated volunteers show boosting of pre‐existing antigen‐specific memory B ‐cell (m BC ) responses following CHMI . In contrast, unvaccinated malaria‐naive control volunteers developed an m BC response against MSP 1 but not AMA 1. Serum I g G correlated with the m BC response after booster vaccination but this relationship was less well maintained following CHMI . A significant reduction in peripheral MSP 1‐specific m BC was observed at the point of diagnosis of blood‐stage infection. This was coincident with a reduction in peripheral blood B ‐cell subsets expressing CXCR 3 and elevated serum levels of interferon‐ γ and CXCL 9, suggesting migration away from the periphery. 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These CHMI data confirm that m BC and antibody responses can be induced and boosted by blood‐stage parasite exposure, in support of epidemiological studies on low‐level parasite exposure.</abstract><doi>10.1111/imm.12226</doi><tpages>17</tpages></addata></record>
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title Analysis of human B ‐cell responses following C h A d63‐ MVA MSP 1 and AMA 1 immunization and controlled malaria infection
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