Hou Nan, Jiang Ning, Zou Yang, Piao Xianyu, Liu Shuai, Li Shanshan, Chen Qijun
MOH Key Laboratory of Systems Biology of Pathogens, Institute of Pathogen Biology, Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing, China.
Key Laboratory of Zoonosis, Shenyang Agriculture UniversityShenyang, China.
Front Microbiol. 2017 Aug 2;8:1431. doi: 10.3389/fmicb.2017.01431. eCollection 2017.
T-cell immunoglobulin and mucin-domain-containing molecule 3 (Tim-3) has complicated roles in regulating monocytes and macrophages in various diseases and it tends to be an inhibitory molecule to facilitate the immune escape of parasites in malaria. However, the mechanisms of Tim-3 mediated responses in monocytes and macrophages in malaria have not been clear. In this study, we found that infection down-regulated Tim-3 expression in peripheral monocytes of patients suffering from malaria and in splenic macrophages of ANKA-infected mice. Tim-3 signal blockade with anti-Tim-3 antibodies enhanced phagocytosis and parasitical mediator production of murine splenic macrophages during infection. In conclusion, Tim-3 constricts monocytes/macrophages activity, and anti-Tim-3 treatment facilitates parasite clearance, especially in the early stage of infection.
T细胞免疫球蛋白黏蛋白结构域分子3（Tim-3）在多种疾病中调节单核细胞和巨噬细胞时发挥着复杂作用，在疟疾中它往往作为一种抑制性分子促进寄生虫的免疫逃逸。然而，Tim-3在疟疾中介导单核细胞和巨噬细胞反应的机制尚不清楚。在本研究中，我们发现感染会下调疟疾患者外周血单核细胞以及ANKA感染小鼠脾脏巨噬细胞中Tim-3的表达。在感染期间，用抗Tim-3抗体阻断Tim-3信号可增强小鼠脾脏巨噬细胞的吞噬作用和寄生虫介质的产生。总之，Tim-3会限制单核细胞/巨噬细胞的活性，抗Tim-3治疗有助于清除寄生虫，尤其是在感染早期。
