Systemic lupus erythematosus (SLE) is a prototype of humansystemic autoimmune diseases. Although the definite etiopathogenesisof SLE remains unclear, many different mechanisms may contributeto the pathogenesis of SLE.A defect in the inhibitory molecules including CTLA4 is onepossibility. As soluble CTLA4 molecule (sCTLA4) was found inhuman serum, it may enhance or inhibit T-cells immune response. Inaddition, previous report had identified a CTLA4 gene polymorphismin promoter sequence with a C to T transition at position 318 (Liu etal., 2003).Aim of the work:The aim of this work is to study the CTLA4 genepolymorphism and the expression of sCTLA4 molecule in patientswith SLE to investigate their possible association with thepathogenesis and susceptibility to the disease.Results:There was significant increased expression of sCTLA4 in SLEpatients compared to controls. However there was no correlation withdisease activity or CTLA4 polymorphism.