الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Systemic lupus erythematosus is a chronic autoimmune disorder of the connective tissue .The pathogenesis of SLE is still unclear, however abnormal immune tolerance and over activation of T and B lymphocytes are the main causes with heterogeneous spectrum of manifestations that affect almost all organ systems (i.e., skin, kidney, joints, cardiovascular, and nervous system).
The exact etiology of SLE is unknown however, multiple factors have been linked with disease development; they include genetic, epigenetic, immunoregulatory, hormonal, and environmental factors.
The structural MHC elements are indirectly related to the initiation of an autoimmune response that can reside in the peptide- binding groove, also in its proximity, within the area directly in contact with the T-cell receptor. The MHC polymorphism in this region may cause either binding of autoreactive effector T cells or weak selection of regulatory T cells. The HLA region is a key genetic factor conferring risk of SLE. Despite multiple SLE association signals identified in the HLA region, only amino-acid residues within HLA- DRB1 have been specifically described.
In the current study, assessment of HLA-DP Gene Polymorphisms (SNPs rs3077 and rs9277535) and its association with the Susceptibility