CD163 is an endocytic receptor mainly expressed in a subpopulation of macrophages. It serves as a scavenger receptor, with a quantitatively important ligand being the haptoglobin-hemoglobin complex. CD163 is involved in multiple biological processes, including endocytosis, phagocytosis, and signaling during inflammation. It is also part of the TWEAK/Fn14/CD163 axis which controls various cellular events such as proliferation, migration, and apoptosis [1,2].

In a study using ApoE -/- CD163 -/- mice, CD163+ macrophages were found to inhibit vascular calcification through NF-κB-induced hyaluronan synthase (HAS) augmentation, promoting the development of high-risk atherosclerotic plaques. The absence of CD163 in these mice led to greater vascular calcification, indicating the role of CD163+ macrophages in restraining this process [3].

In conclusion, CD163 is a crucial receptor in macrophages, playing a significant role in inflammation-related processes and disease development. The use of gene-knockout mouse models, like the ApoE -/- CD163 -/- mice, has provided valuable insights into the role of CD163 in vascular calcification and atherosclerotic plaque development, highlighting its importance in understanding these disease mechanisms.

References:

1. Skytthe, Maria K, Graversen, Jonas Heilskov, Moestrup, Søren K. 2020. Targeting of CD163+ Macrophages in Inflammatory and Malignant Diseases. In International journal of molecular sciences, 21, . doi:10.3390/ijms21155497. https://pubmed.ncbi.nlm.nih.gov/32752088/

2. Ratajczak, Wiktoria, Atkinson, Sarah D, Kelly, Catriona. 2021. The TWEAK/Fn14/CD163 axis-implications for metabolic disease. In Reviews in endocrine & metabolic disorders, 23, 449-462. doi:10.1007/s11154-021-09688-4. https://pubmed.ncbi.nlm.nih.gov/34542797/

3. Sakamoto, Atsushi, Kawakami, Rika, Mori, Masayuki, Virmani, Renu, Finn, Aloke V. 2023. CD163+ macrophages restrain vascular calcification, promoting the development of high-risk plaque. In JCI insight, 8, . doi:10.1172/jci.insight.154922. https://pubmed.ncbi.nlm.nih.gov/36719758/