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Role of γ-Interferon in Induction of Foxp3 and Conversion of CD4+CD25- T cells to CD4+ Regulatory T Cells
Wang Zhaojun 1,Hong Jian 2,Sun Wei 2,Xu Guangwu 1,Li Ningli 1,Chen Xi 1,Liu Ailian 1,Xu Lingyun 1,Sun Bing 1,Zang Jingwu 1 *
1.Shanghai Jiaotong University School of Medicine
2.Department of Neurology, Baylor College of Medicine, Houston, USA
*Correspondence author
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Funding: Chinese Ministry of Science and Technology,National Natural Science Foundation,(No.2002AA216121,202CCCD2000,NSF-30430650,NSF-30571731)
Opened online:16 January 2009
Accepted by: none
Citation: Wang Zhaojun,Hong Jian,Sun Wei.Role of γ-Interferon in Induction of Foxp3 and Conversion of CD4+CD25- T cells to CD4+ Regulatory T Cells[OL]. [16 January 2009] http://en.paper.edu.cn/en_releasepaper/content/27933
 
 
γ−Interferon (γ−IFN) is an important Th1 pro-inflammatory cytokine and has a paradoxical effect on experimental autoimmune encephalomyelitis (EAE) in which the disease susceptibility is unexpectedly heightened in γ−IFN deficient mice. In this study, we provided new evidence indicating that γ−IFN was critically required for the conversion of CD4+CD25- T cells to CD4+ regulatory T cells during EAE. The study showed that the added severity of EAE in γ−IFN knockout mice was directly associated with altered encephalitogenic T cell responses, which correlated with reduced frequency and function of CD4+CD25+Foxp3+ regulatory T cells when compared to wild-type mice. It was demonstrated in both human and mouse systems that in vitro γ−IFN treatment of CD4+CD25- T cells converted to CD4+ regulatory T cells characterized by increased expression of Foxp3 and enhanced regulatory function. Mouse CD4+CD25- T cells, when treated in vitro with γ−IFN, acquired marked regulatory properties as evidenced by suppression of EAE by adoptive transfer. The findings have important implications for the understanding of the complex role of γ−IFN in both induction and self regulation of inflammatory processes.
Keywords:Transcription factor Foxp3; γ-interferon; Experimental autoimmune
 
 
 

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