近来研究表明感染或肿瘤能诱导表达γδTCR的新型髓系细胞亚群，但其特征、作用及形成机制并不明确。我们在疟原虫感染C57BL/6小鼠的多个脏器发现CD3-γδTCR+细胞，其中肺脏最为明显。该细胞群高表达CD11b、CD11c和F4/80等髓系细胞相关分子，不表达CD4、CD8和CD19等淋巴细胞相关分子。该细胞群CD80、MHCⅡ、CD62L、NKG2A/C/E和NKG2D等分子的表达水平；以及IL-1、IL-2和IL-6等细胞因子的分泌能力与其他髓系细胞差别显著。本项目拟从细胞形态、分化成熟、活化及趋化分子表达、细胞因子分泌等方面进一步明确这群CD3-γδTCR+细胞的特点；通过细胞过继转移，明确其在疟原虫致病过程中的作用；通过差异性基因的筛选、体外信号阻滞及基因敲除小鼠，探讨其活化与分化的分子机制。本项目将进一步提高对肺脏δTCR+髓系细胞的认识，为疟疾的防治提供帮助。

Recent reports indicated that a group of γδTCR expressed myeloid cells could be induced by infection or tumor. However, it is still unclear on the feature, function, or mechanism of the development of this cell population. A group of CD3- γδTCR+ cells was found in many tissues and organs, especially in the lungs, of C57BL/6 mice infected by plasmodium in our previous study. In this cell population, high levels of myeloid cells related molecules, CD11b, CD11c and F4/80, no T/B cell related molecules, CD4, CD8 and CD19 was expressed. Moreover, in CD3- CD11b+ cell population, it was significantly different between γδTCR- and γδTCR+ cell groups as to the expression of function associated molecule, CD80, MHCⅡ, CD62L, NKG2A/C/E, and NKG2D; and the ability in cytokines (IL-1、IL-2, and IL-6) secreting. This project intends to further define the phenotypic and functional character of the CD3- γδTCR+CD11b+ myeloid cells from different aspects, including: cellular morphology, maturation, activation, chemotaxis, production of cytokines, and so on; to evaluate the role of this cell population in the mechanism of malaria by the means of δTCR+ myeloid cells adoptive transfer; to explore the molecular mechanism of activation and differentiation of this cell population by the means of genetic screening, in vitro signal blocking, and gene knockout mice. This project will improve the understanding of myeloid cells, and provide help for prevention and control of malaria in the world.