| Popis: |
Kupffer cells play important roles in the modulation of immune response, phagocytosis, and senescent cell removal [1,2]. Hydrolytic enzymes and reactive species produce the killing effects of Kupffer cells and some degree of adjacent tissue damage [1,3]. Liver macrophages are constantly exposed to antigens from portal circulation, to which development of full inflammatory response is useless and potentially harmful [4]. Neither tissue damage nor inflammation follows senescent cell removal by Kupffer cells, due to the physiological control of inflammation events during antigen processing [2,5]. Apolipoproteins can modulate macrophage function [6]. Among them, beta2-glycoprotein I (beta2GPI) decreases Kupffer cells respiratory burst while increases efficiency of C. albicans killing [7]. Beta2GPI also binds phosphatidylserine (PS) residues on the surface of senescent cells, targeting them to clearance [8]. In order to get an insight on the role of beta2GPI in the silent antigen removal by Kupffer cells, perfused mouse liver was used as a model of Kupffer cell-dependent phagocytosis and related respiratory burst activity, and results were correlated with those obtained in isolated mouse non-parenchymal cells. |
Full text from SpringerLink