菌群影响2型免疫反应

Microbiota and Type 2 immune responses

doi 10.1016/j.coi.2018.05.009

Current Opinion in Immunology上发表的一篇综述，介绍了不同部位的菌群（包括肠道和皮肤）如何调节2型免疫反应，并在过敏性疾病中起到重要作用。

论文摘要

The human body is home to trillions of microbes that play a critical role in educating the immune system. This microbiota is a complex community of microorganisms that includes bacteria, archaea, fungi, viruses (including bacteriophages), and protozoa species [1]. All mucosal surfaces, including the gastrointestinal (GI) tract, skin, oral mucosa and lung, are colonized by microbes, although the colon of the GI tract exhibits the highest density and complexity. Microbial colonization is a dynamic process throughout the first years of life that is heavily influenced by external factors, such as mode of birth, diet, breast vs formula feeding, and antibiotic use, and ultimately leads to relatively stable microbial com- munity in adults. The microbiome plays a dominant role in shaping development of the immune system and helps to regulate and fine-tune immune responses. Distur- bances in microbial composition, termed dysbiosis, are associated with many chronic diseases including allergic disease, Inflammatory Bowel Disease (IBD), cancer, and autoimmunity (reviewed in [2]). Although microbial dys- biosis could be a consequence of disease, it is also possible that alterations in the microbiota could occur prior to disease onset and may even be a primary driver of disease pathogenesis. In this short review, we discuss recent murine and human studies that provide insight into the role of the microbiota in inducing, regulating, or prevent- ing Type 2 immune responses. We highlight key studies from the past two years and discuss how they have advanced our view of the pervasive interactions of the microbiota and Type 2 immune responses, particularly during the early life ‘window of opportunity’. 

实验综述

① 菌群通过调节Treg、上皮细胞、树突细胞、天然免疫细胞（ILC）等细胞类群调控2型免疫反应；

② 生命早期的菌群定殖对2型免疫的调节十分重要，在出生后的第0-10天，杯状细胞相关抗原通道（GAP）尚未形成，免疫系统较少暴露于肠道菌群抗原；

③ 出身后第10-20天，在乙酰胆碱的刺激下GAP形成，诱导抗原特异性Treg的产生；

④ 早期肠道菌群的组成差异（例如梭状芽胞杆菌）与食物过敏相关；

⑤ 金黄色葡萄球菌或通过释放丝氨酸蛋白酶诱发过敏性皮肤炎。