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Cage change of mice with persistent murine astrovirus infection triggers stress responses marked by corticosterone fluctuation, which is followed by CD8 T cell activation and induction of epithelial antiviral responses leading to viral clearance.

In response to infection with Staphylococcus aureus in vitro and in vivo, host cells increase their secretion of exosomes containing ADAM10—vesicular structures that can provide protection by sequestering bacterial toxins.

Commensal bacteria are known to have an important role in keeping the host healthy, but the role of eukaryotic viruses has been unknown; now, persistent infection in mice with various strains of enteric norovirus is shown to provide similar host protection.

Pucella, Maqueda-Alfaro and colleagues distinguish three developmentally related subsets of mouse plasmacytoid dendritic cells that differ in their ability to produce type I interferon and their susceptibility to virus.

Here, the authors show that SARS-CoV-2 infection causes gut microbiome dysbiosis and gut epithelial cell alterations in a mouse model, and correlate dysbiosis observed in COVID-19 patients with blood stream infections, matching reads of bacterial sequences from stool samples to organisms found in the blood.

Intraepithelial lymphocytes expressing γ and δ T cell receptor subunits protect Paneth cells from cell death caused by viral infection or Crohn's disease.

Murine norovirus protects intestinal epithelial cells (IECs) from chemical injury by inducing a type I interferon (IFN-I) response in the colon via the viral non-structural protein NS1/2. IFN-I signalling in IECs, in turn, stimulates the production and signalling of the cytoprotective cytokine interleukin-22.

Autophagy-deficient murine hosts are protected from infection and injury at the intestinal barrier and this is driven by a microbiota-dependent type I interferon response, indicating that autophagy is important for limiting host responses to the microbiota.

Here the authors develop a neonatal mouse model for SARS-CoV-2 transmission, characterize differences in viral replication and shedding of variants of concerns, and show that deletion of ORF8 shifts viral replication to the lower respiratory tract and delays transmission.

Oyesola and colleagues show that rewilding mice reveals how genotype and environment combine to determine interindividual immune variation.

In this Review, the authors discuss the gene–environment interactions including microbial perturbations that shape the early events of inflammatory bowel disease.

Both the yeast and hyphal forms of Candida albicans enable colonization of the mammalian gut, with hyphal cells secreting the toxin candidalysin to inihibit bacteria and support fungal commensalism.

This article provides a comprehensive overview of the general functions of autophagy in immunity, the interactions between autophagy and immune signalling pathways and the role of autophagy–immune crosstalk in multicellular immune responses and disease.

High or multiple doses of macrolide antibiotics, when given early in life, can perturb the metabolic and immunological development of lab mice. Here, Ruiz et al. show that even a single macrolide course, given early in life, leads to long-lasting changes in the gut microbiota and immune system of mice.

Pulsed doses of antibiotics increased the incidence of type 1 diabetes in non-obese diabetic (NOD) mice. This was associated with altered gut microbial composition, lipid metabolism, host cholesterol biosynthetic gene expression and Th17 and Treg cell proportions.

Here Ramanan and colleagues provide an analysis of mammary T cells during late pregnancy and lactation. This revealed an increase in intraepithelial lymphocytes in the lactating mammary gland, which was driven by thymic and intestinal inputs and was sensitive to changes in the microbiota

This Review provides insights for construction of molecular cell atlases and outlines key study design considerations. The authors emphasize the power of single-cell and single-nucleus genomics in revealing cellular transitions during nervous system development and disease.

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