γδT细胞通过直接杀伤和吞噬作用抑制恶性疟原虫的血液感染阶段，这一成果由美国波士顿儿童医院Judy Lieberman和Caroline Junqueira团队经过不懈努力而取得。该项研究成果发表在2021年1月11日出版的《自然-免疫学》上。

研究人员发现感染的红细胞（iRBCs）被磷酸化抗原传感器butyrophilin 3A1（BTN3A1）标记。 γδ2T细胞以接触、磷酸抗原、BTN3A1和脱粒依赖的方式形成免疫突触并裂解iRBC，从而杀死细胞内的疟原虫。颗粒溶解酶释放到突触中溶解iRBCs，并向该疟原虫递呈了诱导死亡的颗粒酶。尽管所有红细胞内的疟原虫均易感，但其裂殖体最敏感。因此，γδ2T细胞的次生保护机制得以鉴别。

在存在患者血清的情况下，γδ2T细胞以CD16依赖的方式吞噬并降解了细菌受调理的iRBC，从而减少了疟原虫的繁殖。因此，γδ2T细胞有两种控制疟疾血液感染阶段的方法–γδT细胞抗原受体（TCR）介导的脱粒和抗体包被iRBC的吞噬作用。

研究人员表示，在恶性疟原虫感染患者中会发生由疟原虫诱导的磷酸抗原活化Vγ9Vδ2（γδ2）T淋巴细胞的扩增。尽管先前的研究表明γδ2T细胞有助于控制红细胞疟疾，但仍不确定γδ2T细胞是否识别iRBCs。

附：英文原文

Title: γδ T cells suppress Plasmodium falciparum blood-stage infection by direct killing and phagocytosis

Author: Caroline Junqueira, Rafael B. Polidoro, Guilherme Castro, Sabrina Absalon, Zhitao Liang, Sumit Sen Santara, ngela Crespo, Dhelio B. Pereira, Ricardo T. Gazzinelli, Jeffrey D. Dvorin, Judy Lieberman

Issue&Volume: 2021-01-11

Abstract: Activated Vγ9Vδ2 (γδ2) T lymphocytes that sense parasite-produced phosphoantigens are expanded in Plasmodium falciparum–infected patients. Although previous studies suggested that γδ2 T cells help control erythrocytic malaria, whether γδ2 T cells recognize infected red blood cells (iRBCs) was uncertain. Here we show that iRBCs stained for the phosphoantigen sensor butyrophilin 3A1 (BTN3A1). γδ2 T cells formed immune synapses and lysed iRBCs in a contact, phosphoantigen, BTN3A1 and degranulation-dependent manner, killing intracellular parasites. Granulysin released into the synapse lysed iRBCs and delivered death-inducing granzymes to the parasite. All intra-erythrocytic parasites were susceptible, but schizonts were most sensitive. A second protective γδ2 T cell mechanism was identified. In the presence of patient serum, γδ2 T cells phagocytosed and degraded opsonized iRBCs in a CD16-dependent manner, decreasing parasite multiplication. Thus, γδ2 T cells have two ways to control blood-stage malaria–γδ T cell antigen receptor (TCR)-mediated degranulation and phagocytosis of antibody-coated iRBCs.

DOI: 10.1038/s41590-020-00847-4

Source: https://www.nature.com/articles/s41590-020-00847-4