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Pancreatic α and β cells have different cell autonomous signatures; this explains why α but not β cells can clear infections by potentially diabetogenic viruses.

Retinal ganglion cell axons release the morphogen sonic hedgehog which signals through astrocytes to induce the migration of inhibitory interneurons into the developing visual thalamus.

Combinations of transcription factors can convert pancreatic acinar cells into endocrine α-, β- and δ-cells in vivo.

A conserved transcriptional signature in macrophages and endothelial cells occurs in multiple organs in response to COVID-19 and suggests potential molecular interactions between the two cell types.

We are writing to comment on the study by Meyer et al., 2016 on disease-ameliorating autoantibodies.

Intersectional genetic tools are used for selective control of enteroendocrine cell subtypes in vivo, revealing their differential roles in gut physiology and feeding behavior.

ECM-Itgb1 signaling and cell-cell adhesion are pivotal and coordinate together to regulate pancreatic islet aggregation, architecture, and functional maturation during development.

Single-cell RNA-sequencing, spatial genomics, and histological analyses reveal that cold-induced brown adipose neogenesis is a complex adaptive response to elevated metabolic demand involving dynamic interactions between recruited immune cells and a subpopulation of poised adipocyte progenitors.

Enteroendocrine cells sense nutrients in the gut and regulate digestive physiology but are rendered insensitive following fat ingestion due to alteration of gut microbiota.