Intrinsic Resistance of Hepatocytes to Complement-Mediated Injury
| Autor: | Kiyoshi Ogata, Cody A. Koch, Kim A. Butters, Akiyoshi Kanazawa, Ryuta Nishitai, Bruce E. Knudsen, Timothy B. Plummer, Jeffrey L. Platt |
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| Rok vydání: | 2005 |
| Předmět: |
Cytotoxicity
Immunologic Programmed cell death Swine Immunology Cell Antibodies Heterophile Biology medicine Animals Humans Immunology and Allergy Complement Activation Cells Cultured PI3K/AKT/mTOR pathway Loss function Complement Inactivator Proteins Complement System Proteins Immunity Innate Complement system Complement (complexity) Cell biology medicine.anatomical_structure Immunoglobulin M Immunoglobulin G Hepatocytes Binding Sites Antibody Endothelium Vascular Complement component 5a Function (biology) Signal Transduction |
| Zdroj: | The Journal of Immunology. 174:7302-7309 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.174.11.7302 |
| Popis: | When activated on or in the vicinity of cells, complement usually causes loss of function and sometimes cell death. Yet the liver, which produces large amounts of complement proteins, clears activators of complement and activated complexes from portal blood without obvious injury or impaired function. We asked whether and to what extent hepatocytes resist injury and loss of function mediated by exposure to complement. Using cells isolated from porcine livers as a model system, we found that, in contrast to endothelial cells, hepatocytes profoundly resist complement-mediated lysis and exhibit normal synthetic and conjugative functions when complement is activated on their surface. The resistance of hepatocytes to complement-mediated injury was not a function of cell surface control of the complement cascade but rather an intrinsic resistance of the cells dependent on the PI3K/Akt pathway. The resistance of hepatocytes to complement might be exploited in developing approaches to the treatment of hepatic failure or more broadly to the treatment of complement-mediated disease. |
| Databáze: | OpenAIRE |
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