Abstract
Until recently, studies of natural killer (NK) cells in infection have focused almost entirely on their role in viral infections. However, there is an increasing awareness of the potential for NK cells to contribute to the control of a wider range of pathogens, including intracellular parasites such as Plasmodium spp. Given the high prevalence of parasitic diseases in the developing world and the devastating effects these pathogens have on large numbers of vulnerable people, investigating interactions between NK cells and parasitized host cells presents the opportunity to reveal novel immunological mechanisms with the potential to aid efforts to eradicate these diseases. The capacity of NK cells to produce inflammatory cytokines early after malaria infection, as well as a possible role in direct cytotoxic killing of malaria-infected cells, suggests a beneficial impact of NK cells in this disease. However, NK cells may also contribute to overproduction of pro-inflammatory cytokines and the consequent immunopathology. As comparatively little is known about the role of NK cells later in the course of infection, and growing evidence suggests that heterogeneity in NK cell responses to malaria may be influenced by KIR/HLA interactions, a better understanding of the mechanisms by which NK cells might directly interact with parasitized cells may reveal a new role for these cells in the course of malaria infection.
Highlights
Natural killer (NK) cells are a subset of lymphocytes that contribute to the control of cancers and infections through the production of pro-inflammatory cytokines and the destruction of damaged, dysfunctional or infected host cells via cytotoxic activity [reviewed in Ref. [1]]
Regardless of the underlying mechanism, this raises the intriguing possibility that NK cells may contribute substantially to immune responses after malaria vaccination, and preliminary studies have already demonstrated enhanced NK cell activation in response to increased T cell IL-2 production in individuals vaccinated with the RTS,S/AS01 malaria vaccine [26]
In considering the potential role of killer cell immunoglobulin-like receptor (KIR) in controlling NK cell responses to malaria, more definitive evidence is required for direct, functional interactions between NK cells and infected erythrocytes, and it is necessary to consider that genetic associations between malaria severity and KIR might be mediated by NK cell interactions with infected hepatocytes during the pre-erythrocytic liver stage of infection
Summary
Natural killer (NK) cells are a subset of lymphocytes that contribute to the control of cancers and infections through the production of pro-inflammatory cytokines and the destruction of damaged, dysfunctional or infected host cells via cytotoxic activity [reviewed in Ref. [1]]. Traditionally classed as innate lymphocytes, recent work has suggested that NK cells may participate in adaptive immune responses and may exhibit immunological “memory” or “memory-like” responses leading to significantly higher cytokine production and enhanced cytotoxic responses upon restimulation. Regardless of the underlying mechanism, this raises the intriguing possibility that NK cells may contribute substantially to immune responses after malaria vaccination, and preliminary studies have already demonstrated enhanced NK cell activation in response to increased T cell IL-2 production in individuals vaccinated with the RTS,S/AS01 malaria vaccine [26]. We summarize the current state of knowledge of the role of NK cells during malaria infection and malaria vaccination, both in humans and in experimental murine infections
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