The ontogeny and maturation of the immune system is modulated by the microbiota. During fetal life, the mother’s microbiota produces compounds that are transferred to the fetus and offspring, and enhance the generation of innate immune cells. After birth, the colonizing microbiota induces the development of intestinal lymphoid tissues and maturation of myeloid and lymphoid cells, and imprints the immune system with a reactivity level that persists long after weaning into adulthood. When the cross-talk between host and microbiota is perturbed early in life, a pathological imprinting may develop that is characterized by excessive immune reactivity in adulthood, which translates into increased susceptibility to inflammatory pathologies. In this review, we discuss the recent data that demonstrate the existence of a time window of opportunity early in life during which mice and human have to be exposed to microbiota in order to develop a balanced immune system. We also discuss the factors involved in imprinting, such as the microbiota, immune cells and stromal cells, as well as the nature of imprinting.

免疫系统的个体发育和成熟受微生物群调节。在胎儿期，母亲的微生物群产生的化合物会转移给胎儿和后代，并增强先天免疫细胞的生成。出生后，定植的微生物群会诱导肠道淋巴组织的发育以及骨髓细胞和淋巴细胞的成熟，并给免疫系统留下一个反应水平的印记，这种反应水平在断奶至成年期后仍会持续很长时间。当宿主和微生物群之间的相互作用在生命早期受到干扰时，可能会形成一种病理印记，其特征是成年后免疫反应过度，这会转化为对炎症病理的易感性增加。在这篇评论中，我们讨论了最近的数据，这些数据表明在生命早期存在一个机会时间窗，在此期间小鼠和人类必须接触微生物群才能形成平衡的免疫系统。我们还讨论了印记所涉及的因素，例如微生物群、免疫细胞和基质细胞，以及印记的性质。