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Review
. 2015 Oct 1;11(10):e1005118.
doi: 10.1371/journal.ppat.1005118. eCollection 2015 Oct.

Interferon-γ: The Jekyll and Hyde of Malaria

Thayer King  1 , Tracey Lamb  1
Affiliations
Review

Interferon-γ: The Jekyll and Hyde of Malaria

Thayer King et al. PLoS Pathog. .
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Effector mechanisms induced by IFN-γ during malaria.
Various immune cell subsets produce IFN-γ in response to Plasmodium infection. NK, γδ, and NKT cells are largely responsible for early production of IFN-γ in response to liver and blood stages of the parasite and play a role in early control of parasite growth. IFN-γ-producing CD8+ T cells have also been shown to limit intrahepatic parasite growth through an IFN-γ-inducible, nitric oxide-dependent mechanism (1). Once an adaptive immune response is initiated, IFN-γ produced by CD4+ T cells optimally activates CD8+ T cells, B cells, and macrophages. IFN-γ influences isotype switching in B cells leading to production of cytophilic antibodies capable of binding free parasites and blocking red blood cell invasion (2), mediating parasite clearance through opsonization (3), and binding the surface of infected red blood cells promoting antibody-dependent phagocytosis (4). Production of IFN-γ from CD4+ T cells also optimally activates macrophages to phagocytose infected red blood cells and free parasites (5). All of these mechanisms are important for optimal control of parasite growth during Plasmodium infection.
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