Linkage between innate immunity and adaptive immunity during pahogen infection

病原性感染导致先天免疫的激活，随后诱导Th 1 T细胞亚群。然而，这种转变的机制尚未阐明。我们使用DO 11.10 OVA特异性TCR-TG小鼠T细胞和细胞内感染性病原体单核细胞增生李斯特菌（Lm）来评估病原性感染的效果。我们研究了参与宿主-病原体相互作用的基因，以及在病原体感染的早期阶段启动T细胞亚群分化所需的基因。我们在这份报告中表明，Toll样受体（TLR）-2，TLR-4和MyD 88分子并不是Lm感染过程中诱导Th 1分化所必需的。它还表明，参与Lm的致病性的表达的基因是不需要的诱导Th 1。通过插入转座子或温度敏感质粒，对Lm突变株进行了检测。我们评估了突变体用于确定负责诱导T细胞移位的基因。我们发现Lm突变体的Th 1诱导能力和Th 2诱导抑制能力均丧失，提示Lm基因组中Th 1亚群的诱导和Th 2亚群的诱导抑制是两种不同的现象，受不同基因的影响。

Pathogenic infections lead to activation of innate immunity followed by induction of a Th1 T cell subset. However, the mechanism in this shift has not been clarified. We used DO 11.10 OVA-specific TCR-TG mouse T cell and the intracellular infectious pathogen Listeria monocytogenes (Lm) to evaluate the effect of pathogenic infections. We investigated genes that involved in the host-pathogen interaction and is required for the initiation of T cell subset differentiation in the early phase of pathogen infection. We show in this report that toll like receptor (TLR)-2, TLR-4 and MyD88 molecules are not essentially required for the induction of Th1 differentiation during Lm infection. It is also shown that genes involved in the expression of the pathogenicity of Lm are not required for the induction of Th1. We checked the mutant strain of Lm which were disrupted gene by insertion of transposon or temperature sensitive plasmid. We evaluated the mutant for determining gene(s) responsible for inducing T cell shift. We found the mutants of Lm lost either the ability of Th1 induction or the inhibition of Th2 induction, suggesting that the induction of Th1 subset and the inhibition of Th2 subset induction are separate phenomenon and are influenced by distinct genes carried by Lm genome.