- Published
- 2023-08-01
- Venue
- Clinical Science, vol. 137, no. 15, pp. 1067-1093
- Cited by
- 616
- Open access
- Yes, hybrid
- DOI
- 10.1042/cs20220531
- PubMed
- 37530555
Abstract
Macrophages represent heterogeneous cell population with important roles in defence mechanisms and in homoeostasis. Tissue macrophages from diverse anatomical locations adopt distinct activation states. M1 and M2 macrophages are two polarized forms of mononuclear phagocyte in vitro differentiation with distinct phenotypic patterns and functional properties, but in vivo, there is a wide range of different macrophage phenotypes in between depending on the microenvironment and natural signals they receive. In human infections, pathogens use different strategies to combat macrophages and these strategies include shaping the macrophage polarization towards one or another phenotype. Macrophages infiltrating the tumours can affect the patient's prognosis. M2 macrophages have been shown to promote tumour growth, while M1 macrophages provide both tumour-promoting and anti-tumour properties. In autoimmune diseases, both prolonged M1 activation, as well as altered M2 function can contribute to their onset and activity. In human atherosclerotic lesions, macrophages expressing both M1 and M2 profiles have been detected as one of the potential factors affecting occurrence of cardiovascular diseases. In allergic inflammation, T2 cytokines drive macrophage polarization towards M2 profiles, which promote airway inflammation and remodelling. M1 macrophages in transplantations seem to contribute to acute rejection, while M2 macrophages promote the fibrosis of the graft. The view of pro-inflammatory M1 macrophages and M2 macrophages suppressing inflammation seems to be an oversimplification because these cells exploit very high level of plasticity and represent a large scale of different immunophenotypes with overlapping properties. In this respect, it would be more precise to describe macrophages as M1-like and M2-like.
Cite this paper
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- APA 7
Strizova, Z. O., Benešová, I., Bartolini, R., Novysedlák, R., Cecrdlova, E., Foley, L. K., & Střı́ž, I. (2023). M1/M2 macrophages and their overlaps – myth or reality? Clinical Science, 137(15), 1067–1093. https://doi.org/10.1042/cs20220531
- MLA 9
Strizova, Zuzana Ozaniak, et al. "M1/M2 macrophages and their overlaps – myth or reality?" Clinical Science, vol. 137, no. 15, 2023, pp. 1067–1093, https://doi.org/10.1042/cs20220531.
- Chicago
Strizova, Zuzana Ozaniak, Iva Benešová, Robin Bartolini, René Novysedlák, Eva Cecrdlova, Lily Koumbas Foley, and Ilja Střı́ž. "M1/M2 macrophages and their overlaps – myth or reality?" Clinical Science 137, no. 15 (2023): 1067–1093. https://doi.org/10.1042/cs20220531.
- GOST
Strizova Z. O., Benešová I., Bartolini R. [и др.] M1/M2 macrophages and their overlaps – myth or reality? // Clinical Science. — 2023. — Vol. 137, № 15. — P. 1067–1093. — URL: https://doi.org/10.1042/cs20220531
- BibTeX
@article{strizova2023macrophages, title = {{M1/M2 macrophages and their overlaps – myth or reality?}}, author = {Zuzana Ozaniak Strizova and Iva Benešová and Robin Bartolini and René Novysedlák and Eva Cecrdlova and Lily Koumbas Foley and Ilja Střı́ž}, journal = {Clinical Science}, year = {2023}, volume = {137}, number = {15}, pages = {1067--1093}, doi = {10.1042/cs20220531}, url = {https://doi.org/10.1042/cs20220531} }- RIS
TY - JOUR AU - Strizova, Zuzana Ozaniak AU - Benešová, Iva AU - Bartolini, Robin AU - Novysedlák, René AU - Cecrdlova, Eva AU - Foley, Lily Koumbas AU - Střı́ž, Ilja TI - M1/M2 macrophages and their overlaps – myth or reality? JO - Clinical Science VL - 137 IS - 15 SP - 1067 EP - 1093 PY - 2023 DA - 2023/08/01 DO - 10.1042/cs20220531 UR - https://doi.org/10.1042/cs20220531 ER -
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