Genotoxic stress signalling as a driver of macrophage diversity

Affiliations:

¹ Department of Rheumatology and Clinical Immunology and Institute of Microbiology, Charité University Medical Center, D-10117 Berlin, Germany.

² German Rheumatism Research Center, a Leibniz Institute, D-10117 Berlin, Germany.

Keywords: 

DNA damage, ATR, ATM, innate immunity, macrophage programs, chronic inflammation.

Abbreviatons:

AGS – Aicardi-Goutieres Syndrome;

ATM – Ataxia telangiectasia mutated;

ATR – Ataxia telangiectasia and Rad3-related;

BMDM – bone marrow-derived macrophage;

cGAS – cyclic GMP-AMP synthase;

DDR – DNA Damage Response;

DNA-PK – DNA-dependent protein kinase;

DNA-PKcs – DNA-PK catalyitc subunit;

dNTP – deoxynucleoside triphosphate;

ds – double strand;

HR – homologous recombination;

IFN – interferon;

IL – interleukin;

IRF – IFN regulatory factor;

LPS – lipopolysaccharide;

MCMV – murine cytomegalovirus;

MCSF – macrophage colony stimulating factor;

MRN – Mre11-Rad50-NBS1;

NHEJ – non-homologous end joining;

NK – natural killer;

NO – nitric oxide;

RAG – recombination-activated gene;

ROS – reactive oxygen species;

ss – single strand;

SCID – severe combined immunodeficiency;

STING – stimulator of interferon genes;

TLR – toll-like receptor.

Corresponding Author(s):

Conflict of interest statement:

The authors certify that they have no affiliations with or involvement in any organization or entity with any financial or non-financial interest in the subject matter or materials discussed in this manuscript.

Please cite this article as:

Ana Kasapi and Antigoni Triantafyllopoulou (2022). Genotoxic stress signalling as a driver of macrophage diversity. Cell Stress 6(3): 30-44. doi: 10.15698/cst2022.03.265

© 2022 Kasapi and Triantafyllopoulou. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and re-production in any medium, provided the original author and source are acknowledged.