Who on IRF are you? IRF8 deficiency redirects cDC1 lineage commitment

Kathryn Waller; Charlotte L Scott

doi:10.1016/j.it.2022.07.007

Who on IRF are you? IRF8 deficiency redirects cDC1 lineage commitment

Trends Immunol. 2022 Sep;43(9):687-689. doi: 10.1016/j.it.2022.07.007. Epub 2022 Aug 10.

Authors

Kathryn Waller¹, Charlotte L Scott²

Affiliations

¹ Laboratory of Myeloid Cell Biology in Tissue Damage and Inflammation, VIB Center for Inflammation Research, Ghent, Belgium; Department of Biomedical Molecular Biology, Faculty of Sciences, Ghent University, Ghent, Belgium.
² Laboratory of Myeloid Cell Biology in Tissue Damage and Inflammation, VIB Center for Inflammation Research, Ghent, Belgium; Department of Biomedical Molecular Biology, Faculty of Sciences, Ghent University, Ghent, Belgium; Department of Chemical Sciences, Bernal Institute, University of Limerick, Castletroy, Limerick, Ireland. Electronic address: charlotte.scott@ugent.be.

PMID: 35963772
DOI: 10.1016/j.it.2022.07.007

Abstract

Interferon regulatory factor 8 (IRF8) has long been associated with conventional dendritic cell type I (cDC1) development. In a recent study, Lança et al. demonstrate that IRF8 is also crucial in cells already committed to the cDC1 lineage. Here, deletion of IRF8 from the XCR1-expressing pre-cDC1 stage onward leads to a loss of commitment and reprogramming of the cells toward a cDC2-like phenotype.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Animals
Dendritic Cells*
Interferon Regulatory Factors*
Mice
Mice, Inbred C57BL

Substances

Interferon Regulatory Factors