Volume 2, Issue 2 (Autumn – Winter 2009[PERSIAN] 2008)                   mljgoums 2008, 2(2): 0-0 | Back to browse issues page

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Abedian S, Mirabi A, Parsaee M. The Effect of Interferon Beta in HLA-G Expression on Monocyte in Diabetes Type1. mljgoums 2008; 2 (2)
URL: http://mlj.goums.ac.ir/article-1-50-en.html
1- Immunologist, Assistant Professor , abedianlab@yahoo.co.uk
Abstract:   (15865 Views)
Abstract Background and objectives: Dendritic Cells are the most important of antigen presenting cells with an effective role in immune tolerance. This study, aims to clarify the role of IFN- β in induction on dendritic cells derived by monocyte in diabetes type1 to evaluate the T cells response to beta cell specific antigenic molecule. Material and Methods: In this research, peripheral blood mononuclear cells were isolated by phiCole and then dendritic cells generated from blood monocytes ,in Seven days, by adding granulocyte-monocyte colony stimulating factor and interleukin-4 with or without IFN-beta. MRNA was extracted by dendritic cells and cDNA was produced by reverse transcriptase enzyme. Then, Specific polymerase chain reaction for HLA-G was performed. In addition, Tcell proliferation with a mixed Leukocytic reaction evaluated between dendritic cell and T by means of MTT. Results: based on the results, IFN-β induces HLA-G molecule on dendritic cells. In addition, T cell proliferation responses in mixed leukocyte culture show significance difference between Case and control p<0.05. T cell proliferation was inhibited in their co-culture system affected by IFN-β Conclusion: In this study, we show that dendritic cells-treated IFN-β with expression of HLA-G molecule inhibited T cell proliferation and so, our results suggest that some of the IFN- β regulatory effects with expression of HLA-G can probably prevent from beta cell destruction. Key words: dendritic cells, Interferon Beta, Human Leukocytic Antigen-G.

Received: 2011/08/27 | Accepted: 2014/01/12 | Published: 2014/01/12 | ePublished: 2014/01/12

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This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.