Type I IFN signaling shapes subset-specific monocyte fates in the injured myocardium
Abstract
Monocytes and macrophages promote tissue repair following myocardial infarction, but the mechanisms tuning their effector functions remain elusive. While macrophages are essential in clearing debris and resolving inflammation, they can also contribute to uncontrolled inflammation and provoke additional damage. Thus, factors that influence macrophage differentiation trajectories and phenotypes play an important role in cardiac repair outcomes. By combining genetic lineage tracing with cell-specific targeting, the study from Koenig et al. sheds light on key signaling events that shape monocyte fate decisions in the injured myocardium, establishing a differentiation hierarchy among monocyte-macrophage subsets. The findings also reveal that macrophages with an IFN response signature give rise to MHCIIhi macrophages, which, in turn, contribute to regulatory T cell generation and cardioprotection. This work underscores the importance of understanding cardiac macrophage phenotypic plasticity within a broader framework of lineage relationships.
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BibTeX
@article{sakalli2026type,
title = {{Type I IFN signaling shapes subset-specific monocyte fates in the injured myocardium}},
author = {Ecem Tugba Sakalli and Giuseppe Rizzo and Alma Zernecke and Gustavo Campos Ramos},
journal = {The Journal of clinical investigation},
year = {2026},
month = sep,
doi = {10.1172/jci209791},
url = {https://hal.science/hal-05780638v1},
note = {CC BY},
}
RIS
TY - JOUR
TI - Type I IFN signaling shapes subset-specific monocyte fates in the injured myocardium
AU - Ecem Tugba Sakalli
AU - Giuseppe Rizzo
AU - Alma Zernecke
AU - Gustavo Campos Ramos
PY - 2026
DA - 2026/09/01
JO - The Journal of clinical investigation
DO - 10.1172/jci209791
UR - https://hal.science/hal-05780638v1
AB - Monocytes and macrophages promote tissue repair following myocardial infarction, but the mechanisms tuning their effector functions remain elusive. While macrophages are essential in clearing debris and resolving inflammation, they can also contribute to uncontrolled inflammation and provoke additional damage. Thus, factors that influence macrophage differentiation trajectories and phenotypes play an important role in cardiac repair outcomes. By combining genetic lineage tracing with cell-specific targeting, the study from Koenig et al. sheds light on key signaling events that shape monocyte fate decisions in the injured myocardium, establishing a differentiation hierarchy among monocyte-macrophage subsets. The findings also reveal that macrophages with an IFN response signature give rise to MHCIIhi macrophages, which, in turn, contribute to regulatory T cell generation and cardioprotection. This work underscores the importance of understanding cardiac macrophage phenotypic plasticity within a broader framework of lineage relationships.
SN - 1558-8238
ER -