Type I Interferons Regulate Immune Responses in Humans with Blood-Stage Plasmodium falciparum Infection
Marcela Montes de(The University of Queensland), Rajiv Kumar(QIMR Berghofer Medical Research Institute), Fabian de Labastida Rivera(QIMR Berghofer Medical Research Institute), Fiona H. Amante(QIMR Berghofer Medical Research Institute), Meru Sheel(QIMR Berghofer Medical Research Institute), Rebecca J. Faleiro(Queensland University of Technology), Patrick T. Bunn(Griffith University), Shannon E. Best(QIMR Berghofer Medical Research Institute), Lynette Beattie(QIMR Berghofer Medical Research Institute), Susanna S. Ng(Griffith University), Chelsea L. Edwards(The University of Queensland), Glen M. Boyle(QIMR Berghofer Medical Research Institute), Ric N. Price(Charles Darwin University), Nicholas M. Anstey(Charles Darwin University), Jessica R. Loughland(Charles Darwin University), Julie G. Burel(QIMR Berghofer Medical Research Institute), Denise L. Doolan(QIMR Berghofer Medical Research Institute), Ashraful Haque(QIMR Berghofer Medical Research Institute), James McCarthy(The University of Queensland), Christian Engwerda(QIMR Berghofer Medical Research Institute)
Cited by 106Open Access
Abstract
T cell IFNγ production, and they promoted the development of parasitic-specific IL-10-producing Th1 (Tr1) cells. Type I IFN-dependent, parasite-specific IL-10 production was also observed in P. falciparum malaria patients in the field following chemoprophylaxis. Parasite-induced IL-10 suppressed inflammatory cytokine production, and IL-10 levels after drug treatment were positively associated with parasite burdens before anti-parasitic drug administration. These findings have important implications for understanding the development of host immune responses following blood-stage P. falciparum infection, and they identify type I IFNs and related signaling pathways as potential targets for therapies or vaccine efficacy improvement.
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