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Author Notes:
Email Address: tracey.j.lamb@emory.edu
The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
The authors have declared that no competing interests exist.
Subjects:
Research Funding:
National Institute for Neurological Disorders and Stroke (1R21N5085382-01A1)
Emory University Immunology and Molecular Pathogenesis training grant (5T32AI007610-15)
Royal Society
Emory Egleston Children's Research Center
Interferon-γ: The Jekyll and Hyde of Malaria
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.
Copyright information:
© 2015 King, Lamb.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits distribution of derivative works, making multiple copies, distribution, public display, and publicly performance, provided the original work is properly cited. This license requires copyright and license notices be kept intact, credit be given to copyright holder and/or author.
