PDF(Pubmed)
Abstract：
Through immune memory, infections have a lasting effect on the host. While memory cells enable accelerated and enhanced responses upon rechallenge with the same pathogen, their impact on susceptibility to unrelated diseases is unclear. We identify a subset of memory T helper 1 (Th1) cells termed innate acting memory T (TIA) cells that originate from a viral infection and produce IFN-γ with innate kinetics upon heterologous challenge in vivo. Activation of memory TIA cells is induced in response to IL-12 in combination with IL-18 or IL-33 but is TCR independent. Rapid IFN-γ production by memory TIA cells is protective in subsequent heterologous challenge with the bacterial pathogen Legionella pneumophila. In contrast, antigen-independent reactivation of CD4+ memory TIA cells accelerates disease onset in an autoimmune model of multiple sclerosis. Our findings demonstrate that memory Th1 cells can acquire additional TCR-independent functionality to mount rapid, innate-like responses that modulate susceptibility to heterologous challenges.
摘要：
通过免疫记忆，感染对宿主有持久的影响。虽然记忆细胞能够在用相同的病原体再次攻击时加速和增强反应，它们对无关疾病易感性的影响尚不清楚.我们鉴定了记忆T辅助1（Th1）细胞的子集，称为先天作用记忆T（TIA）细胞，其起源于病毒感染，并在体内异源攻击时产生具有先天动力学的IFN-γ。记忆TIA细胞的活化是响应于IL-12与IL-18或IL-33的组合而诱导的,但不依赖于TCR。记忆TIA细胞的快速IFN-γ产生在随后与细菌病原体嗜肺军团菌的异源攻击中是保护性的。相比之下,在多发性硬化的自身免疫模型中,CD4+记忆TIA细胞的抗原非依赖性再激活加速疾病的发作.我们的发现表明，记忆Th1细胞可以获得额外的TCR无关功能，调节对异源挑战的易感性的先天样反应。
