Linkage between innate immunity and adaptive immunity during pahogen infection

病原性感染导致先天免疫激活，然后诱导Th1T细胞亚群。然而，这一转变中的机制尚未得到澄清。我们用DO 11.10 OVA特异的TCR-TG小鼠T细胞和细胞内感染病原菌单核细胞增多性李斯特菌(Listeria moncytogiate，Lm)来评价病原性感染的效果。我们研究了参与宿主-病原体相互作用的基因，这些基因是在病原体感染的早期阶段启动T细胞亚群分化所必需的。在本报告中，我们发现Toll样受体(TLR)-2、TLR-4和MyD88分子并不是诱导LM感染过程中Th1分化所必需的分子。研究还表明，参与LM致病性表达的基因并不是诱导Th1所必需的。我们对通过插入转座子或温度敏感质粒而导致基因中断的突变株进行了检测。我们对决定导致T细胞转移的基因(S)的突变体进行了评估。我们发现突变体失去了诱导Th1或抑制Th2的能力，这表明诱导Th1亚群和抑制Th2亚群诱导是两个独立的现象，并且受LM基因组携带的不同基因的影响。

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.