Imprinting of the immune system by the microbiota early in life

被引:164
|
作者
Al Nabhani, Ziad [1 ]
Eberl, Gerard [1 ]
机构
[1] Inst Pasteur, Microenvironm & Immun Unit, INSERM, U1224, Paris, France
关键词
T-CELL DIFFERENTIATION; GUT MICROBIOTA; ANTIBIOTIC-TREATMENT; SUSCEPTIBILITY; TOLERANCE; INNATE; MEMORY; DYSBIOSIS; EXPOSURE; DISEASE;
D O I
10.1038/s41385-020-0257-y
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:183 / 189
页数:7
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