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The development of immunoregulatory networks is important to prevent disease. However, these same networks allow pathogens to persist and reduce vaccine efficacy. Here, we identify type I interferons (IFNs) as important regulators in developing anti-parasitic immunity in healthy volunteers infected for the first time with Plasmodium falciparum. Type I IFNs suppressed innate immune cell function and parasitic-specific CD4+ 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.

Original publication

DOI

10.1016/j.celrep.2016.09.015

Type

Journal article

Journal

Cell Rep

Publication Date

04/10/2016

Volume

17

Pages

399 - 412

Keywords

CD4(+) T cells, Th1 cells, Tr1 cells, immune regulation, malaria, type I interferons, Antiparasitic Agents, CD4-Positive T-Lymphocytes, Healthy Volunteers, Host-Parasite Interactions, Humans, Immunity, Innate, Interferon Type I, Interferon-gamma, Interleukin-10, Malaria, Falciparum, Plasmodium falciparum, Th1 Cells