الفهرس 
INTRODUCTION&Aim of the workOnly 14 pages are availabe for public view
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Abstract
RA is one of the commonest chronic inflammatory diseases, characterized by inflammation of the synovium and pannus formation in the diseased joint, which may lead to eventual degradation of the articular cartilage and the . subchondral bone (Albani and Carson, 1997). GM-CSF is one of the haematopoietic cytokines that could be crucial to pathogenesis of RA as it is potent macrophage activator including the induction of HLA-DR expression, tumouricidal activity, IL-I secretion, intracellular parasite killing and priming for enhanced release ofTNF-u and PG-E2. Neutrophil function is also regulated by GM-CSF which enhances antibody dependent cytotoxicity, phagocytosis, chemotaxis and production of oxygen radicles (Firestein, 1997). Furthermore, the role of IFN-y as an inducer ofHLA-DR in chronic disease appears to have been supplanted by other cytokines espically GM-CSF (Alvaro-Garcia et al., 1989). The aim of this study was to explore and integrate the role of GM -CSF in RA and, to assess its relation to clinical and laboratory parameters of this disease.