Table of contents

Volume 6, Issue 3, pp. 30 - 44, March 2022

Issue cover
Cover: This month in Cell Stress: COX4-1 in mitochondrial supercomplex assembly. Image depicts cell with nucleus (blue) and mitochondria (green). Image credit: NICHD/U. Manor, via Flickr CC BY 2.0 license. Image modified by Cell Stress. The cover is published under the CC BY 4.0 license. Enlarge issue cover


Genotoxic stress signalling as a driver of macrophage diversity

Ana Kasapi and Antigoni Triantafyllopoulou

page 30-44 | 10.15698/cst2022.03.265 | Full text | PDF | Abstract

Tissue macrophages arise from yolk sac, fetal liver and hematopoietic progenitors and adopt diverse transcriptional programs and phenotypes, instructed by their microenvironment. In chronic inflammation, such as in chronic infections, autoimmunity, or cancer, tissue microenvironments change dramatically thus imprinting new programs on tissue macrophages. While stress is a known driver of carcinogenesis in epithelial cells, emerging evidence suggests that macrophage responses to genotoxic stress are embedded in their ‘physiologic’ immune and tissue healing programs and in most cases do not lead to myeloid malignancies. The role of genotoxic stress as an instructor of macrophage-mediated immune defense and tissue remodeling is only beginning to be understood. Here, we review the evidence showing that genotoxic stress, which macrophages and their precursors face upon encountering inflammatory and/or growth signals, instructs their transcriptional programs, by activating non-canonical, cell-type specific DNA Damage Response (DDR)-driven signaling pathways. We propose that immune-cell specific, DDR-instructed programs are crucial for tissue homeostasis as well as for the maintenance and resolution of inflammatory responses in infection, cancer, autoinflammatory and autoimmune microenvironments.

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