There can now be no doubt that interactions between multicellular organisms and the microbial species with which they coexist are of profound importance to both the host and to their complex coexisting communities. When technological breakthroughs in microbial sequencing first began to revolutionize our understanding of host–microbial interactions, it was exciting to learn about the numerous associations between changes in microbial communities and concomitant alterations in the status of their hosts, be these nutritional, environmental or pathological. As the catalog of associations grew, investigators began to also define causal relationships. Commonly, changes in the host environment affect their microbiota. Importantly, changes in key individual species or in the community structure and functions of the microbiota can also affect the host. These microbial changes, often acting through now well‐defined molecular mechanisms, impact the host immune response. Interactions with the intestinal microbiota can not only affect the outcome of enteric infections, but also influence immunological homeostasis, and thus influence conditions that may not previously have been considered to be intestine related.

Collaborative and enjoyable discussions between the teams at Immunology, a journal of the British Society for Immunology, and Immunology & Cell Biology (ICB), the flagship journal of the Australian and New Zealand Society for Immunology, revealed a wealth of high‐quality and well‐received articles investigating interactions with the microbiome in both journals. This prompted us to develop a joint Virtual Issue (i.e. “Immunology and the Microbiome”) highlighting our excellent microbiome research. Six articles from each journal are featured in this Virtual Issue.1-12 We will highlight the ICB articles here. The companion articles in Immunology are described in our accompanying Editorial in Immunology.13

The ICB articles cover a wide range of topics, from reviews describing mechanistic interactions with components of the immune system,1, 2 through original articles describing novel molecular interactions with the microbiota and their influence on inflammation3 and vaccine responses,4 to investigations of the relationships between the microbiota and diabetes in NOD mice,5 and in patients with stroke.6

Two of the ICB articles are reviews discussing interactions between the host, the microbiota and pathogenic microorganisms.1, 2 The influence of the microbiota on the development of both adaptive memory and innate “memory” is the focus of the review by McCoy et al., which is placed in the topical context of vaccine efficiency (Figure 1①).1 Meermeier et al. discuss the influence of infectious microorganisms on mucosal‐associated invariant T cells, the “most abundant T‐cell subset in humans” (Figure 1②).2

Much has been learned recently about specific host–microbial interactions. For example, Alteber at al. show how mice that lack the interferon‐inducible transmembrane protein 3 (IFITM3) gene are not only more susceptible to bacteria‐dependent experimental colitis, but also have significantly different microbiota from their littermates before colitis is induced (Figure 1③).3

In some circumstances, careful investigation reveals elements of the immune response that are not affected by changes in the intestinal microbiota. We include two examples in this series.4, 5 First, Poyntz et al. examine the antibody response to immunization in substrains of BALB/c mice and find that changes in the intestinal microbiota do not affect the substrains’ different antibody response phenotypes (Figure 1④).4 Instead, they identify genetic polymorphisms affecting isotype class‐switching that are differentially expressed in mice from different vendors. Second, Mullaney et al. show how the stable inter‐relationship between host and microbiota can be difficult to perturb, frustrating efforts to identify the causal factors driving pathology (Figure 1⑤).5 They show that cohousing diabetes‐susceptible mice, from birth, with resistant C57BL/6 mice that have different intestinal microbiota has little effect on the development of pathogenic CD8 T cells.

The final article in this ICB collection, a review from Malone et al. investigates the contributions of the immune response to the pathogenesis of stroke (Figure 1⑥).6 As an integral part of this, the authors discuss how the gut microbiota may influence the inflammatory environment, and discuss the exciting potential for stroke immunotherapies.

To complement these ICB papers, there are six papers in Immunology. Zhao and Elson begin by investigating how the seeding of the microbiota after birth can affect lifelong health, and ask whether the microbiota can be manipulated to reduce susceptibility to inflammatory disease.7 This question of the therapeutic potential of microbial manipulation is critically important. Gudi et al. provide an answer to this question, providing a complex dietary polysaccharide “prebiotic” to modulate T cells and suppress type 1 diabetes in non‐obese diabetic mice.8 Such immune‐modulatory effects may be mediated by bacterial metabolic products. The review by Haase et al. focuses on how short‐chain fatty acids and tryptophan metabolites in particular influence both the immune system and the brain, potentially affecting neuroinflammatory conditions such as multiple sclerosis.9 Of course, interactions between the microbiota and the immune system are bidirectional and multifactorial. For instance, Singh et al. show that the absence of eosinophils changes the diversity of mucus‐associated intestinal microbial communities,10 while Kehrmann et al. demonstrate that loss of regulatory T cells can increase the abundance of intestinal bacteria of the Firmicutes phylum.12 Furthermore, Hoces et al. describe how soluble immunoglobulin A may simultaneously both prevent disease and enable bacterial colonization, by “enchaining” or clumping dividing bacteria.11 This may have a number of effects, impacting local microbial evolution by both reducing horizontal microbial gene transfer and selectively influencing clonal growth and death.

We are excited to present these articles, in this joint Virtual Issue with Immunology, and are grateful to all our authors for their contributions. We invite you to explore the series and enjoy learning more about the details of this fascinating work.

毫无疑问，多细胞生物与其共存的微生物物种之间的相互作用对宿主及其复杂的共存群落都具有深远的意义。当微生物测序的技术突破首次开始彻底改变我们对宿主 - 微生物相互作用的理解时，了解微生物群落变化与其宿主状态随之发生的变化之间的众多关联令人兴奋，无论是营养、环境还是病理。随着关联目录的增加，调查人员也开始定义因果关系。通常，宿主环境的变化会影响它们的微生物群。重要的是，关键个体物种或微生物群落结构和功能的变化也会影响宿主。这些微生物变化通常通过现在明确的分子机制起作用，影响宿主的免疫反应。与肠道微生物群的相互作用不仅会影响肠道感染的结果，还会影响免疫稳态，从而影响以前可能与肠道无关的条件。

协作和团队在之间愉快的讨论免疫学，英国社会为免疫学杂志，和免疫学，细胞生物学（ICB），澳大利亚和新西兰社会为免疫学的旗舰期刊，发现了丰富的高品质和良好- 在这两种期刊上收到了研究与微生物组相互作用的文章。这促使我们开发了一个联合虚拟问题（即“免疫学和微生物组”），以突出我们出色的微生物组研究。来自每个期刊的六篇文章在这个虚拟问题上有特色。1-12我们将在这里重点介绍ICB文章。免疫学的配套文章在我们随附的免疫学社论中进行了描述。13

的ICB的文章涵盖广泛主题，从评论描述与免疫系统的组分机械相互作用1,2通过描述与微生物群和它们对炎症的影响新的分子相互作用原始制品3和疫苗应答，4到的调查NOD 小鼠5和中风患者的微生物群与糖尿病之间的关系。6

在两个ICB文章评论讨论主机，微生物和病原微生物之间的相互作用。1, 2微生物群对适应性记忆和先天“记忆”发展的影响是 McCoy等人评论的重点，该评论被置于疫苗效率的主题背景下（图 1①）。1梅尔迈尔等人。讨论传染性微生物对黏膜相关不变 T 细胞的影响，这是“人类最丰富的 T 细胞亚群”（图 1②）。2

最近已经了解了很多关于特定宿主-微生物相互作用的知识。例如，Alteber at al。显示缺乏干扰素诱导跨膜蛋白 3 ( IFITM3 ) 基因的小鼠不仅对细菌依赖性实验性结肠炎更敏感，而且在诱导结肠炎之前与同窝小鼠具有显着不同的微生物群（图 1③）。3

在某些情况下，仔细研究揭示了不受肠道微生物群变化影响的免疫反应要素。我们在本系列中包含两个示例。4, 5首先，Poyntz等人。检查 BALB/c 小鼠亚系对免疫的抗体反应，发现肠道微生物群的变化不影响亚株的不同抗体反应表型（图 1④）。4相反，他们确定了影响同种型转换的遗传多态性，这些遗传多态性在来自不同供应商的小鼠中差异表达。二、穆拉尼等人. 显示宿主和微生物群之间稳定的相互关系如何难以扰乱，令人沮丧的努力确定驱动病理的因果因素（图 1⑤）。5他们表明，从出生起，将糖尿病易感小鼠与具有不同肠道微生物群的抗性 C57BL/6 小鼠共住对致病性 CD8 T 细胞的发育几乎没有影响。

此ICB 合集中的最后一篇文章，来自 Malone等人的评论。研究免疫反应对中风发病机制的贡献（图 1⑥）。6作为其中的一个组成部分，作者讨论了肠道微生物群如何影响炎症环境，并讨论了中风免疫疗法的令人兴奋的潜力。

为了补充这些ICB论文，免疫学中有六篇论文。赵和埃尔森首先研究出生后微生物群的播种如何影响终生健康，并询问是否可以操纵微生物群以降低对炎症疾病的易感性。7微生物操作的治疗潜力这个问题至关重要。古迪等人。为这个问题提供答案，提供一种复杂的膳食多糖“益生元”来调节 T 细胞并抑制非肥胖糖尿病小鼠的 1 型糖尿病。8这种免疫调节作用可能是由细菌代谢产物介导的。Haase等人的评论. 重点关注短链脂肪酸和色氨酸代谢物如何影响免疫系统和大脑，从而可能影响多发性硬化等神经炎症。9当然，微生物群和免疫系统之间的相互作用是双向和多因素的。例如，辛格等人。表明不存在嗜酸性粒细胞的改变粘液相关的肠道微生物群落的多样性，10而Kehrmann等。证明调节性 T 细胞的丧失可以增加厚壁菌门肠道细菌的丰度。12此外，Hoces等人. 描述可溶性免疫球蛋白 A 如何通过“束缚”或聚集分裂细菌，同时预防疾病和促进细菌定植。11这可能会产生多种影响，通过减少微生物基因水平转移和选择性影响克隆生长和死亡来影响当地微生物进化。

我们很高兴在这个与免疫学联合的虚拟问题中展示这些文章，并感谢我们所有作者的贡献。我们邀请您探索这个系列，并享受更多地了解这部引人入胜的作品的细节。