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Abstract Acute rheumatic fever is (l systemic inflammatory disease thought to be immunological in origin and resulting from a previous group A streptococcal pharyngeal infection. There is strong evidence that the pathogenesis of rheumatic fever in susceptible individuals results from an abnormal host immune response, of humoral or cellular typc or both, to streptococcal antigens (Zahrislde, 1985). Cytokines are known to have an important role in inflammation and autoimll1une reactions (Relll icl{, 1997). In rheumatic fever, the immuno-inflalllmatory response is triggered by a streptococcal antigen. The antigen is presented hy APC to R Iymphocytes. T-cells may be helper or suppressive and responsible with the macrophages for the reaction of cytokines. The objectives of this work in to investigate the gene expression by determination of mRNA and estimation or serum levels of IL-4, and IL¬10. Ilso to study lhe possible genetic tendcncy The study included 146 children, out or them 89 were patients with rheunllltjc fever (RP), 7 suffering from streptococcal pharyngitis (SP), and 50 heallhy children taken as control group. Children were taken up consecutively from the cardiology unit qf the MUCH.The total (146 children) was enrolled into the following groups: Grollp I: 29 with active rheumatic hem! discnsc (ARll!). Grollp 2: 8 with acutc rhcumatic fcvcr mthritis (ARF 1). |