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Kupffer cells (KC), the resident liver macrophages, constitute the liver sinusoids together with other cells such as sinusoidal endothelial cells, hepatic stellate cells, liver-specific natural killer cells and dendritic cells. KC account for approximately 10–15% of the total liver cell population and represent 80–90% of tissue macrophages in the reticuloendothelial system. KC represent an important component of innate immunity.1 2 One characteristic of innate immunity is the rapid response to potentially dangerous stimuli. This suggests a central role of the liver in systemic and regional immune response, because KC come in contact with all the microbiological debris from the gastrointestinal tract reaching the liver via the portal vein.3
KC express the scavenger receptor CD163; CD163 is involved in the clearance and endocytosis of the haemoglobin–haptoglobin complex.4 Once erythrocytes or the haemoglobin–haptoglobin complex has been taken up by KC, the heme delivered from haemoglobin is degraded by heme oxygenases. The isoform heme oxygenase-1 is only observed in KC and its expression and the consecutive bilirubin production increases immediately after exposure to damaged erythrocytes. Heme oxygenase-1 and CD163 expression increase after exposure to inflammatory stimuli. The interplay of KC, CD163 and heme oxygenase-1 has thus been identified as an important system that is upregulated in inflammatory conditions in order to enhance haemoglobin clearance and heme degradation.5
The interesting study …
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Funding The author is supported by the following grants: DFG STE 1022/2-1, DFG STE 1022/2-3, FöFoLe LebMit 133/200 and an unrestricted grant from Norgine.
Competing interests None.
Provenance and peer review Commissioned; not externally peer reviewed.