الفهرس 
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Abstract
The most important autoimmune diseases are rheumatoid arthritis (RA), and systemic lupus
erythematous (SLE). Rheumatoid arthritis (RA) is a chronic, progressive, inflammatory autoimmune disease that is associated with articular, extra-articular and systemic effects. Systemic lupus erythematous (SLE) is a disorder of immune regulation resulting in chronic inflammation that affects many organs with the production of autoantibodies. Tumor necrosis factor (TNF-α) may be detrimental in autoimmune diseases, by both inducing inflammation and apoptosis, which could fuel the autoimmune response. TGF- β1 is the most potent naturally occurring immunosuppressant; it plays a fundamental role in controlling proliferation and the fate of cells through apoptosis. The current study was planned to investigate the association between RA, SLE and TNFα, and TGFβ1 polymorphism, in addition the correlation between these polymorphisms and clinical features of RA, and SLE. Detection of TNFα (308 G/A), and TGFβ1 (T869) polymorphisms were detected by using RFLP-PCR were done for 115 subjects whom including 92 autoimmune disease patients divided in to
50 SLE , 42 RA , in addition to 23 healthy control subjects. Susceptibility to RA was significant for homozygote for TNF-α 308 G-allele (GG). While there wasn’t association between SLE, and TNF-α
308 G-allele (GG) genotype. Susceptibility to RA wasn’t significant for homozygote for TGFβ1 T869C T-allele (TT); on the other hand there was association between TGFβ1 T869C T and SLE. Present study reported cases of SLE more common than of RA in youth. Female patients were affected more compared to male patients by RA and SLE. Our results suggest that single nucleotide polymorphism in TNF α at position 308 in which the sequence of nucleotide change from G base in to A base this lead to loss of the normal TNF α function may be involved in the pathogenesis of auto immune disease . 308 G/A TNF α polymorphism was associate with susceptibility to RA, on the other.