Both mouse and human harbour memory phenotype CD8⁺ T cells specific for antigens in hosts that have not been previously exposed to these antigens. The origin and the nature of the stimuli responsible for generation of CD44^hi CD8⁺ T cells in specific pathogen-free (SPF) mice remain controversial. It is known that microbiota plays a crucial role in the prevention and resolution of systemic infections by influencing myelopoiesis, regulating dendritic cells, inflammasome activation and promoting the production of type I and II interferons. By contrast, here we suggest that microbiota has a direct effect on generation of memory phenotype CD44^hiGP33⁺CD8⁺ T cells. In SPF mice, it generates a novel GP33⁺CD44^hiCD8⁺ T cell sub-population associating the properties of innate and genuine memory cells. These cells are highly enriched in the bone marrow, proliferate rapidly and express immediate effector functions. They dominate the response to LCMV and express particular TCRβ chains. The sequence of these selected TCRβ chains overlaps with that of GP33⁺CD8⁺ T cells directly selected by microbiota in the gut epithelium of SPF mice, demonstrating a common selection mechanism in gut and peripheral CD8⁺ T cell pool. Therefore microbiota has a direct role in priming T cell immunity in SPF mice and in the selection of TCRβ repertoires during systemic infection. We identify a mechanism that primes T cell immunity in SPF mice and may have a major role in colonization resistance and protection from infection.

小鼠和人类的港口记忆表型CD8 ⁺ T细胞对宿主中未曾暴露于这些抗原的抗原具有特异性。在特定的无病原体（SPF）小鼠中，负责产生CD44 ^hi CD8 ⁺ T细胞的刺激的起源和性质仍存在争议。众所周知，微生物群通过影响骨髓生成，调节树突状细胞，炎性体活化并促进I型和II型干扰素的产生，在预防和解决全身性感染中起着至关重要的作用。相比之下，在这里我们建议微生物群对记忆表型CD44 ^hi GP33 ⁺ CD8 ^+的产生具有直接影响。T细胞。在SPF小鼠中，它会产生一个新的GP33 ⁺ CD44^喜CD8 ⁺ T细胞亚群的先天和真正的存储单元的属性相关联。这些细胞在骨髓中高度富集，迅速增殖并表达立即的效应子功能。它们控制对LCMV的反应并表达特定的TCRβ链。这些选择的TCRβ链的序列与微生物群在SPF小鼠的肠上皮细胞中直接选择的GP33 ⁺ CD8 ⁺ T细胞的序列重叠，证明了肠道和外周CD8 ⁺的共同选择机制。T细胞池。因此，微生物群在引发SPF小鼠的T细胞免疫以及在系统感染期间选择TCRβ库中具有直接作用。我们确定了启动SPF小鼠中T细胞免疫力的机制，并可能在定植抗性和免受感染中发挥主要作用。