About this Research Topic
Macrophages are highly abundant in all organs and play a vital role in tissue development, maintenance, and surveillance. They have been considered plastic and dynamic cells, rapidly adapting to their changing demands. Indeed, tissue-resident macrophages comprise a highly heterogeneous cell population with various phenotypes and functions according to their inter- and intra-organ-specific location. However, several recent studies have challenged the concept of plasticity by showing that the local tissue microenvironment strongly imprints macrophages with only limited genes being regulated by inflammation. What (micro-)environmental signals enforce tissue imprinting remains largely unknown.
While tissue imprinting equips macrophages with the ability to safeguard tissue homeostasis, this may impair macrophages’ plasticity and ability to fully respond to and clear inflammation. Indeed, early during inflammation, tissue-resident macrophages have been found to be strongly depleted in mice and large numbers of monocytes are recruited that can give rise to macrophages, which replenish organs. These newly recruited macrophages may be necessary to react to inflammatory insults. While some of these newly recruited macrophages are only transient and lost upon inflammation resolution, others remain and become tissue resident. The latter, together with some remaining ‘original’ tissue-resident macrophages, may potentially retain an innate memory of the inflammatory event. If innate memory (trained immunity) affects macrophages capacity to resolve inflammation remains unknown. Similarly, it remains to be resolved which environmental clues signal to macrophages that inflammation has been resolved and that macrophages can return to their homeostatic phenotypes.
The goal of this research topic is to expand the current knowledge regarding the tissue-specific regulation of macrophages in the steady state and inflammation resolution. An understanding of homeostatic tissue imprinting of macrophages may enable the discovery of novel therapeutic targets to promote chronic disease resolution. We welcome Original Research articles and Reviews addressing the following questions:
(1) What are the mechanisms underlying tissue-specific metabolic (lipids, amino acids, sugars, iron) imprinting in steady state?
(2) What are the mechanisms underlying tissue-specific ECM-driven (integrins, cytokines) imprinting in steady state?
(3) What is the impact of tissue-specific imprinting on macrophage plasticity?
(4) How does innate memory affect insult resolution?
(5) Can tissue-specific clues reverse pro-disease phenotypes of macrophages in chronic diseases and can targeting these pathways enable inflammation resolution?
Please Note: Studies on monocytes or other dendritic cells are also suitable for this topic. However, studies addressing how inflammation, cancer, microbiota, circadian rhythm, and central influences imprint myeloid cells are out of scope of this topic. We further do not accept research that only consists of bioinformatics analysis of either public databases or author-generated omics data
While tissue imprinting equips macrophages with the ability to safeguard tissue homeostasis, this may impair macrophages’ plasticity and ability to fully respond to and clear inflammation. Indeed, early during inflammation, tissue-resident macrophages have been found to be strongly depleted in mice and large numbers of monocytes are recruited that can give rise to macrophages, which replenish organs. These newly recruited macrophages may be necessary to react to inflammatory insults. While some of these newly recruited macrophages are only transient and lost upon inflammation resolution, others remain and become tissue resident. The latter, together with some remaining ‘original’ tissue-resident macrophages, may potentially retain an innate memory of the inflammatory event. If innate memory (trained immunity) affects macrophages capacity to resolve inflammation remains unknown. Similarly, it remains to be resolved which environmental clues signal to macrophages that inflammation has been resolved and that macrophages can return to their homeostatic phenotypes.
The goal of this research topic is to expand the current knowledge regarding the tissue-specific regulation of macrophages in the steady state and inflammation resolution. An understanding of homeostatic tissue imprinting of macrophages may enable the discovery of novel therapeutic targets to promote chronic disease resolution. We welcome Original Research articles and Reviews addressing the following questions:
(1) What are the mechanisms underlying tissue-specific metabolic (lipids, amino acids, sugars, iron) imprinting in steady state?
(2) What are the mechanisms underlying tissue-specific ECM-driven (integrins, cytokines) imprinting in steady state?
(3) What is the impact of tissue-specific imprinting on macrophage plasticity?
(4) How does innate memory affect insult resolution?
(5) Can tissue-specific clues reverse pro-disease phenotypes of macrophages in chronic diseases and can targeting these pathways enable inflammation resolution?
Please Note: Studies on monocytes or other dendritic cells are also suitable for this topic. However, studies addressing how inflammation, cancer, microbiota, circadian rhythm, and central influences imprint myeloid cells are out of scope of this topic. We further do not accept research that only consists of bioinformatics analysis of either public databases or author-generated omics data
Keywords: macrophages, dendritic cells, monocytes, steady-state
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
