Abstract
Whether and how γδT cells play a protective role in immunity against Plasmodium infection remain open questions. γδT cells expand in patients and mice infected with Plasmodium spp, and cytokine production and cytotoxic responses against blood-stage parasites are observed in vitro. Their expansion is associated with protective immunity induced by irradiated sporozoite immunization, and depletion of γδT cells in some mouse models of malaria excacerbates blood-stage infections. It is now clear that these cells can have many different functions, and data are emerging suggesting that in addition to having direct parasitocidal effects, they can regulate other immune cells during Plasmodium infections. Here we review some of the historic and more recent data on γδT cells, and in light of the new information on their potential protective roles we suggest that it is a good time to re-evaluate their activation requirements, specificity and function during malaria.
Highlights
Malaria is endemic in large parts of tropical and subtropical countries with high morbidity and mortality
Whether and which coreceptors are engaged in response to Plasmodium is an open question, and worthy of investigation as it may help explain how/why different γδT cells become activated in malaria
For human and mouse γδT cells responding to Plasmodium, costimulation is provided via interaction of CD28 on the γδT cell and CD80 and CD86 on the target/presenting cell
Summary
Malaria is endemic in large parts of tropical and subtropical countries with high morbidity and mortality. Whether and which coreceptors are engaged in response to Plasmodium is an open question, and worthy of investigation as it may help explain how/why different γδT cells become activated in malaria. For human and mouse γδT cells responding to Plasmodium, costimulation is provided via interaction of CD28 on the γδT cell and CD80 and CD86 on the target/presenting cell.
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