结核菌感染可诱导巨噬细胞（MΦ）的活化表型由M1向M2改变来逃避机体免疫杀伤，但其机制不明。我们前期研究发现：①长链非编码RNA(lncRNA) AK140703在M2型MΦ和结核菌感染后期表达上调；②siRNA沉默AK140703后可显著抑制MΦ M2分子的表达；③AK140703沉默后的MΦ受结核菌感染后，其活化表型长期维持M1状态，M2极化受阻。据此推测：AK140703可能通过调控MΦ的极化改变参与结核菌的感染过程。故在此基础上构建结核菌感染MΦ模型和小鼠结核病模型，明确结核菌感染过程中AK140703在MΦ的表达特点及规律；通过RNA干扰和基因过表达等手段，探讨AK140703在结核感染中对MΦ极化表型及抗结核免疫的影响；并应用基因芯片和生物信息学方法筛选AK140703靶基因，阐明其调控MΦ极化改变的分子机制。该研究对了解结核病发病机制及探索新的防治措施具有重要意义。

Mycobacterium tuberculosis infection can induce the activation phenotype of macrophages changing from M1 to M2 to escape immune destruction, but the mechanism is unknown. Our previous study found that the expression of long noncoding RNA (lncRNA) AK140703 will increase in M2 macrophages and the late infection of Mycobacterium tuberculosis; Knockdown of AK140703 by siRNA significantly reduced the expression of M2 molecule; knockdown of AK140703 inmacrophage remained M1 polarization after Mycobacterium tuberculosis infection, and diminished M2 phenotype expression. Therefore we can speculate that AK140703 may play an important role in regulating macrophage polarization duing the infection of Mycobacterium tuberculosis. On this basis, we construct the model of the phenotype of macrophages carried with Mycobacterium tuberculosis and the infected mice, define the characteristic expression and regulation of which AK140703 regulate macrophage polarization in the process of tuberculosis infection; Explore that AK140703 have an effect on the polarization phenotype of macrophages in TB infection and anti-tuberculosis immune through the means of siRNA interference and gene overexpression, and illustrate the molecule mechanism of regulation in macrophage polarization through the methods of gene chip and bioinformatics to Screen target genes of AK140703. The study has important implications for understanding the pathogenetic mechanisms of tuberculosis and to explore new prevention measures.