الفهرس 
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Abstract
Juvenile rheumatoid arthritis (JRA), the most common of the childhood-onset rheumatic disorders, encompasses a spectrum of different diseases that are largely distinct from adult- onset rheumatoid arthritis (RA). Each is thought to be autoimmune in nature. A common feature of autoimmune diseases, such as JeA and SLE, is a dysregulation of normal immune responses which leads to chronic tissue inflammation and damage. Adhesion molecule expression and interactions are probably involved in the initiation and propagation of autoimmune diseases (Laucella et al., 1999). Juvenile rheumatoid arthritis (JRA) is believed to be a complex genetic trait, and involvement of multiple chromosome regions in its susceptibility is anticipated (Sampath et al., 2000). Studies of the genetic component have, for a long time, focused on the HLA genes and resulted in the discovery of a number of associations of autoimmune diseases with alleles of both HLA class I and class II loci (Ploski, 1995). The objectives of this work is to investigate adhesion molecules regarding their serum levels and their gene expression (by determination of mRNA). And to study the possible genetic control of JRA (by HLA subtyping).