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ResearchIn-Press PreviewImmunologyInfectious disease Open Access | 10.1172/jci.insight.199206

Previous malaria exposure attenuates monocyte-driven inflammation and correlates with modulation of the B cell response

Maximilian Julius Lautenbach,1 Pengjun Xi,1 Linn Kleberg,1 Alan-Dine Courey-Ghaouzi,1 Maia Serene Gower,1 Carolina Sousa Silva,1 Felicia Chammas,1 Anna Färnert,1 and Christopher Sundling1

1Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden

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1Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden

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1Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden

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1Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden

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1Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden

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1Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden

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1Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden

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1Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden

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1Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden

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Published September 8, 2026 - More info

JCI Insight. https://doi.org/10.1172/jci.insight.199206.
Copyright © 2026, Lautenbach et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Published September 8, 2026 - Version history
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Abstract

Clinical immunity to malaria develops after repeated malaria episodes. In this process, the inflammatory response is modulated to respond less vigorously upon reinfection. Monocytes are a major source of pro-inflammatory mediators during blood-stage infection and are known to adapt to repeated pathogen exposure. Here, we investigated the impact of previous malaria exposure on monocytes during blood-stage malaria by comparing the response in previously exposed and primary infected individuals. We observed reduced levels of several proinflammatory chemokines in previously exposed individuals, linked to changes in monocytes. Similarly, BAFF levels were lower in these individuals and associated with modulation of monocyte and dendritic cells. This affected the BAFF-BAFF-R axis, crucial for B cell responses, correlating with increasing parasite-specific antibody levels. Collectively, we present insights into how previous malaria exposure shapes monocyte responses during acute malaria and how these in turn correlate with modulation of the B cell compartment and humoral immune response.  

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