Gagliardi Maria Cristina, Lemassu Anne, Teloni Raffaela, Mariotti Sabrina, Sargentini Valeria, Pardini Manuela, Daffé Mamadou, Nisini Roberto
Dipartimento di Malattie Infettive, Parassitarie e Immunomediate, Istituto Superiore di Sanità, Viale Regina Elena 299. 00161, Roma, Italy.
Cell Microbiol. 2007 Aug;9(8):2081-92. doi: 10.1111/j.1462-5822.2007.00940.x. Epub 2007 Apr 17.
We previously described an escape mechanism exploited by Mycobacterium tuberculosis (Mtb) to prevent the generation of fully competent dendritic cells (DC). We have now tested the effect of isolated mycobacterial components on human monocyte differentiation into DC and demonstrated that cell wall (CW)-associated alpha-glucan induces monocytes to differentiate into DC (Glu-MoDC) with the same altered phenotype and functional behaviour of DC derived from Mtb-infected monocytes (Mt-MoDC). In fact, Glu-MoDC lack CD1 molecule expression, fail to upregulate CD80 and produce IL-10 but not IL-12. We also showed that Glu-MoDC are not able to prime effector T cells or present lipid antigens to CD1-restricted T-cell clones. Thus, we propose a mechanism of Mtb-monocyte interaction mediated by CW-associated alpha-glucan, which allows the bacterium to evade both innate and acquired immune responses.
我们之前描述了结核分枝杆菌（Mtb）利用的一种逃逸机制，以阻止完全成熟的树突状细胞（DC）的产生。我们现在测试了分离的分枝杆菌成分对人单核细胞分化为DC的影响，并证明细胞壁（CW）相关的α-葡聚糖可诱导单核细胞分化为DC（Glu-MoDC），其具有与源自Mtb感染单核细胞（Mt-MoDC）的DC相同的改变的表型和功能行为。事实上，Glu-MoDC缺乏CD1分子表达，无法上调CD80并产生IL-10而非IL-12。我们还表明，Glu-MoDC无法启动效应T细胞或向CD1限制性T细胞克隆呈递脂质抗原。因此，我们提出了一种由CW相关的α-葡聚糖介导的Mtb-单核细胞相互作用机制，该机制使细菌能够逃避先天免疫和获得性免疫反应。
