Editors' Summary: This Replication Study has reproduced some parts of the original paper but it also contains results that are not consistent with other parts of the original paper.

Impaired autophagy influences intestinal inflammation and hypersensitivity responses by orchestrating mucosal T cell populations, suggesting new translational perspectives for the treatment of these conditions.

Innate lymphoid cells, which are dynamic under steady-state conditions, respond to a colitogenic stimulus by mobilizing from cryptopatches and secreting GM-CSF to organize the pro-inflammatory response.

A detailed time-series analysis reveals that the interleukin-10 receptor prevents susceptibility to microbiota-driven colonic inflammation that emerges at the time of weaning by directly inhibiting the acquisition of a pro-inflammatory intestinal macrophage phenotype.

Bioinformatics analyses and experiments in mouse models reveal how Escherichia coli accesses the molecular hydrogen pool to boost colonization during acute colitis.

A strategy combining large mouse and human genetic data sheds light on dietary and genetic drivers of gut inflammation.

The sequencing of microbial genomes reveals that the presence of a particular microbial species in the gut may increase the risk of the autoimmune disease rheumatoid arthritis.

Sestrin2 loss could be a universal mechanism of human colon carcinogenesis that allows for barrier dysfunction, mTORC1 hyperactivation, unrestricted tumor growth and chemoresistance.