title: Fas ligation triggers apoptosis in macrophages but not endothelial cells.
abstract: The reticuloendothelial system includes macrophages and endothelial cells. These cells are produced and destroyed in vivo with a precision that implies the existence of homeostatic mechanisms. The stimuli for endothelial cell proliferation and monocyte production are becoming well characterized. However, the mechanisms involved in eliminating these cells are poorly understood. One mechanism involved in cellular elimination is apoptosis, which can be triggered in some cells by ligation of the Fas molecule. In this report we have investigated whether macrophages and endothelial cells express the Fas molecule, and whether Fas transmits an apoptosis-inducing signal in these cells. We demonstrate that macrophages express Fas and readily undergo apoptosis when cultured with anti-Fas. In contrast, while endothelial cells can express the Fas molecule, Fas ligation is insufficient to induce apoptosis. These results suggest differential regulation of Fas function among cells of the reticuloendothelial system, and imply different mechanisms of homeostasis.
authors.affiliation: Department of Internal Medicine, University of Michigan, Ann Arbor.
authors.forename: B C
authors.initials: BC
authors.lastname: Richardson
authors.forename: N D
authors.initials: ND
authors.lastname: Lalwani
authors.forename: K J
authors.initials: KJ
authors.lastname: Johnson
authors.forename: R M
authors.initials: RM
authors.lastname: Marks
mesh_terms: D000954:Antigens, Surface / Q000032:analysis / Q000502:physiology*; D017209:Apoptosis; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology*; D006706:Homeostasis; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000209:etiology; D008264:Macrophages / Q000166:cytology*; D019014:fas Receptor
chemical_list: D000954:Antigens, Surface; D019014:fas Receptor