Malaria is an infectious disease caused by the protozoan parasite , the most lethal being . Clinical malaria is associated with the asexual replication cycle of parasites inside the red blood cells (RBCs) and a dysregulated immune response. Although the mechanisms of immune responses to blood-or liver-stage parasites have been extensively studied, this has not led to satisfactory leads for vaccine design. Among innate immune cells responding to infection are the non-conventional gamma-delta T-cells. The Vγ9Vδ2 T-cell subset, found only in primates, is activated in response to non-peptidic phosphoantigens produced by stressed mammalian cells or by microorganisms such as Mycobacteria, ., and . The potential protective role of Vγ9Vδ2 T-cells against infections and cancer progression is of current research interest. Vγ9Vδ2 T-cells have been shown to play a role in the early control of parasitemia and to influence malaria adaptive immunity cytokine release and antigen presentation. They are activated and expanded during a primary infection in response to malaria phosphoantigens and their activity is modulated upon subsequent infections. Here, we review the wide range of functions by which Vγ9Vδ2 T-cells could both contribute to and protect from malaria pathology, with a particular focus on their ability to induce both innate and adaptive responses. We discuss how the multifunctional roles of these T-cells could open new perspectives on gamma-delta T-cell-based interventions to prevent or cure malaria.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6277687 | PMC |
http://dx.doi.org/10.3389/fimmu.2018.02760 | DOI Listing |
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