الفهرس 
introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
Rheumatoid arthritis is a chronic, inflammatory, debilitating disease and the cause of considerable suffering and economic loss. conventional slow acting drugs are disappointing, so there is a need for a more effective and less toxic drug therapy which might be the basis of improved understanding of pathophysiology of the disease (Rankin et al., 1995).
The unknown antigen incriminated in the pathology of RA is presented by MHC class II positive cells to CD4+ lymphocytes. These are activated and produce lymphokines which recruit more CD4+ cells, B-cells growth factors cause the rapid maturation of B-cells to plasma cells. These secrete rheumatoid factors which form immune complexes, these in turn are phagocytosed by macrophages and polymorphs, leading to further activation. The ensuing release of lysosomal enzymes and formation of reactive oxygen intermediates produce erosion and destruction of cartilage and bone. Release of IL-1 and TNF also cause direct damage to the joint by activating chondrocytes and osteoclasts as well as recruiting other inflammatory cells (Chapel et al., 1999).