الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Kupffer cells are specialized macrophages of the liver form the major part of the reticuloendothelial system and scattered within sinusoids of the liver. They are composed of differentiated monocytes that are originated from the bone marrow (Szymanska and Schmidt-Pospua, 1979; Naito et al., 1997; Stachura and Galazka, 2003). During hepatotoxin-induced liver injury, Kupffer cells and Natural killers are activated. Their activation results in secretion of a large number of pro-inflammatory cytokines such as IL-1, IL-6, IL-8, TNF-α) and different chemokines that can both induce liver injury either by affecting directly on liver tissue cells or through chemoattraction of extrahepatic cells such as neutrophils (PMN) and lymphocytes (Table I.1, Fig. I.1) (Afford and Lalor, 2006; Saile and Ramadori, 2007). The adhesion molecules expression pattern in the Kupffer cells is changed during inflammatory conditions that are induced by TNF-α and IL-6 release and characterized by the downregulation of PECAM-1 and the upregulation of ICAM-1 (Fig. I.1) (Saile and Ramadori, 2007; Neubauer et al., 2008). This leads to migration of the inflammatory cells towards the hepatocytes. It was suggested that the role of the T-lymphocytes in liver injury is performed by activating Kupffer cells to produce TNF-α (Schumann et al., 2000). The hepatocellular stress induced by hepatotoxins may lead to activation of the liver resident macrophages on one side and release of chemokines on the other side.