Interferon-γ: The Jekyll and Hyde of Malaria

• Type of Material: Article
• Authors: Thayer King, Emory University; Tracey Lamb, Emory University
• Language: English
• Date: 2015-10-01
• Publisher: Public Library of Science
• Publication Version: Final Published Version
• Copyright Statement: © 2015 King, Lamb.
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1371/journal.ppat.1005118
• Title of Journal or Parent Work: PLoS Pathogens
• ISSN: 1553-7366
• Volume: 11
• Issue: 10
• Start Page: e1005118
• End Page: e1005118
• Grant/Funding Information: Royal Society; Emory Egleston Children's Research Center; National Institute for Neurological Disorders and Stroke (1R21N5085382-01A1); Emory University Immunology and Molecular Pathogenesis training grant (5T32AI007610-15)
• Research Categories: Health Sciences, Medicine and Surgery; Health Sciences, Immunology; Health Sciences, General

Abstract

Interferon gamma (IFN-γ) is a key mediator of inflammatory immune responses induced primarily by interleukin-12 (IL-12). IFN-γ secretion by both innate and adaptive immune cells is essential for control of intracellular pathogens and tumors, yet aberrant production of IFN-γ contributes to autoimmunity and inflammation in certain disease settings. These divergent roles are well illustrated in the context of malaria, a disease caused by infection with protozoan parasites of the genus Plasmodium. IFN-γ is a central cytokine in controlling Plasmodium infection in both the liver and blood stages of the parasite life cycle, but it can also exacerbate the severity of malarial disease depending on the temporal and spatial production of IFN-γ. Here, we review the types of immune cells that produce IFN-γ during malaria and discuss the IFN-γ-induced effector mechanisms that can aid in killing Plasmodium parasites but also contribute to the pathogenesis of malaria.