The 2nd pathway of T cell subset differentiation induced by pathogenic infection

病原性感染导致先天免疫激活，继而诱导1型T细胞亚群，因此，提供了一个很好的模型来评估T细胞何时承诺为1型T细胞。在这里，我们展示了一个两步机制的T细胞亚群承诺在病原性感染。第一步是由巨噬细胞/树突状细胞的基本功能介导的，不依赖于抗原。这一步骤调节T细胞亚群的承诺前体频率，并影响T-bet(T细胞中表达的T-box)和GATA-3基因的表达。第二步需要联合IL-12或IL-4对T细胞进行抗原刺激，并影响T-bet和GATA-3的表达。基于这些观察结果，我们提出了一个两步T细胞亚群承诺途径。因此，在T细胞遇到名义抗原之前，病原体感染会影响T细胞的功能。

Pathogenic infections lead to activation of innate immunity followed by induction of a type 1 T cell subset, and therefore, provide a good model to evaluate when T cells commit to type 1 T cells. Here we show a two-step mechanism of T cell subsets commitment during pathogenic infection. The first step is mediated by the basal function of macrophage/dendritic cells and is antigen-independent. This step modulates the committed precursor frequency of T cell subsets and influences the expression of T-bet (T-box expressed in T cells ) and GATA-3 genes. The second step requires antigenic stimulation of T cells together with IL-12 or IL-4 and influences on the expression of T-bet and GATA-3. We propose a two-step T cell subset commitment pathway based on these observations. Therefore, pathogenic infections influence on functional T cell commitment before T cells encounter nominal antigen.