Autosomal dominant IRF4 deficiency is the first genetic etiology of Whipple's disease, a very rare chronic condition following a rather common infection by Tropheryma whipplei.

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.

CBP/EP300 bromodomain inhibitors have a therapeutic application in oncology via targeting the IRF4 transcriptional program, a clinically validated network critical for multiple myeloma cell viability.

SPOP-dependent degradation of interferon regulatory factor 1 curtails cell-intrinsic innate immunity, thereby contributing to immune resolution.

HIV-1 Vpr antagonises innate immune sensing of viral and non-viral stimuli by preventing activated IRF3 and NF-κB nuclear transport.

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.

Reprogramming of transcription factors by PRR-independent (cAMP) and PRR-dependent (curdlan) signaling induces new dendritic cell subset.

Endothelial-specific supplementation with Aff3ir-ORF2 significantly ameliorated disturbed flow-induced endothelial activation and the development of atherosclerotic plaques, highlighting its promising therapeutic potential for the treatment of atherosclerosis.

Modeling glioblastoma using expression of relevant human oncogenes in syngeneic zebrafish offers a powerful platform for current and future biological discovery, diagnostics, and therapeutic testing in an intact tumor microenvironment.

A transcriptional coactivator turns into a repressor at specific genes in colorectal cancer cells.