Title of article :
Effect of Estrogen on Th1, Th2 and Th17 Cytokines Production by Proteolipid Protein and PHA Activated Peripheral Blood Mononuclear Cells Isolated from Multiple Sclerosis Patients
Author/Authors :
Javadian، نويسنده , , Ani and Salehi، نويسنده , , Eisa and Bidad، نويسنده , , Katayon and Sahraian، نويسنده , , Mohammad Ali and Izad، نويسنده , , Maryam، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2014
Pages :
6
From page :
177
To page :
182
Abstract :
Background and Aims e body of studies has shown that 17-β estradiol (E2) has a protective effect on susceptibility to experimental autoimmune encephalomyelitis (EAE). Clinical improvement in multiple sclerosis and its animal model, EAE, during pregnancy, when estrogen levels are high, suggests an immunomodulatory role for estrogens. The immune basis for this protection is poorly understood. In this study we evaluated the effect of E2 on the synthesis of inflammatory, antiinflammatory and regulatory cytokines. s lyzed the effect of E2 on IL-4, IL-10, IL-17, TNF-α and IFN-γ cytokines produced by proteolipid protein (PLP) or mitogen phytohemagglutinin (PHA)-activated peripheral blood mononuclear cells isolated from multiple sclerosis patients in comparison to healthy control group. We used RT-PCR and ELISA to detect the level of cytokines. s nd that E2 significantly increased IL-10 expression and secretion and decreased expression of TNF-α in both groups and IL-4 in patients in cells stimulated with PLP or PHA (p <0.0001). sion data indicated that E2 could affect expression and secretion of inflammatory and anti-inflammatory cytokines and could regulate immune responses especially in the differentiation towards regulatory responses, and this finding might have therapeutic value in multiple sclerosis.
Keywords :
Estrogen , MULTIPLE SCLEROSIS , 17-? Estradiol , TH2 , Th17 , Th1 , Regulatory T cells
Journal title :
Archives of Medical Research
Serial Year :
2014
Journal title :
Archives of Medical Research
Record number :
1797962
Link To Document :
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