Mechanism of protective immunity against blood-stage malaria by CD8T cells.

耗尽CD 8 T细胞的小鼠在感染其他非致死性血液期疟疾寄生虫期间显示出较高的寄生虫血症和较低的存活率，表明CD 8 T细胞的保护作用。然而，这些细胞如何介导对感染缺乏MHC I类表达的红细胞的血液阶段疟疾寄生虫的保护是难以捉摸的。在本研究中，我们发现红细胞的祖细胞--成红细胞被疟原虫寄生，并且被寄生的成红细胞以抗原特异性的方式被CD 8 T细胞识别，这表明被寄生的成红细胞是CD 8 T细胞的靶标。我们进一步探讨了CD 8 T细胞发挥的保护机制。我们发现，磷脂酰丝氨酸外化后的CD 8 T细胞上的细胞毒性分子FasL的靶细胞上的Fas，这导致诱导有效的巨噬细胞的吞噬作用的寄生细胞。

Mice depleted of CD8 T cells showed higher parasitemia and lower survival during infection with otherwise non-lethal blood-stage malaria parasites, indicating protective roles of CD8 T cells. However, how these cells mediate protection to blood-stage malaria parasites that infect red blood cells deficient in MHC class I expression is elusive. In this study, we found that erythroblasts, progenitor cells of red blood cells, are parasitized by malaria parasites, and parasitized erythroblasts were recognized by CD8 T cells in an antigen-specific manner, suggesting that parasitized erythroblasts are the target of CD8 T cell. We further explored protective mechanisms exerted by CD8 T cells. We revealed that phosphatidylserine was externalized on parasitized cells after a ligation of cytotoxic molecule FasL on CD8 T cells to Fas on the target cells, which leads to induce effective phagocytosis by macrophages.