Figure 1.

Proposed model of Vγ9Vδ2 T-cell functions in the microvasculature during P. falciparum infection. Plasmodium-infected red blood cells sequester to the endothelium in the microvasculature, where they release phosphoantigens concomitantly with the red blood cell rupture. Phosphoantigens stimulate Vγ9Vδ2 T-cells via BTN3A1 available on neighboring cells, including Vγ9Vδ2 T-cells, the endothelial cells and innate immune cells. Activated Vγ9Vδ2 T-cells (1) modulate innate cells by cytokine secretion, (2) inhibit free parasite reinvasion of red blood cells, by releasing the cytotoxic granulysin, and (3) acquire APC phenotype and the capability to migrate to lymph nodes where they initiate an adaptive immune response.