HDAC3 regulates the development of pDCs and maintenance of homeostasis of hematopoietic progenitors with dendritic cell (DC) differentiation potential, mechanistically by repressing cDC1 associated genes in a deacetylase-dependent manner.

Single-cell RNA-seq data and transgenic models revealed B-plasmacytoid dendritic cells (B-pDCs) represent a phenotypically and functionally distinct common lymphoid progenitor-derived pDC lineage specialized in T cell activation and previously not described in mice.

Cryo-electron microscopy structures of full-length P5CS, the proline synthesis enzyme, reveal that filamentation is crucial for the coordinated catalytic reactions between the glutamate kinase and γ-glutamyl phosphate reductase domains.

A novel lncRNA marks the Irf8 downstream enhancer that is crucial for differentiation of plasmacytoid dendritic cells (pDC) and classical dendritic cells type 1 (cDC1) and confers feedback inhibition of Irf8 transcription.

Probing of various culture conditions leads to fundamental advances in ex vivo production of plasmacytoid dendritic cells for use in immunotherapy.

Cytomegaloviruses are recognized by distinct sensors depending on the infected cell type and together these sensors are essential for viral control and downstream immune responses.

Perivascular extracellular vesicles induce bone repair, and do so via tetraspanin binding to recipient skeletal progenitor cells.

Patterns of monocyte and dendritic cell mobilization and function during human respiratory viral infections are tissue-specific and pathogen-specific, and future studies must perform comparative investigations in blood and the site of infection for a comprehensive assessment of immune responses.

Fluorescent protein-based reporter mouse models revealed that thymic cooperative antigen transfer is mediated by preferential pairing between a particular thymic epithelial cell subset and specific subset(s) of thymic dendritic cells.

In vivo study of arbovirus infections reveals the dominant role of pDC IRF7-signaling in directing both type I and II IFN responses, and leading to viral control.