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International Journal of Biomedical Science
4(1) 52-57
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© 2005 Master Publishing Group
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Original Article
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Neutralization of IL-4 and IFN-γ Facilitates inducing TGF-β-induced CD4+Foxp3+ Regulatory Cells |
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Xiaojuan Tao1, Jilin Ma1, Yonghua Zhang1,Jianning Yu1, Long Cai1, Juhua Wang2,
Song Guo Zheng2
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1 Division of Rheumatology, Immunology and Nephrology, Zhejiang Traditional Chinese Medicine and Western Medicine Hospital, Hangzhou, People′s Republic of China
2 Division of Rheumatology and Immunology, Department of Medicine, University of Southern California, Keck School of Medicine, Los Angeles, USA
Corresponding Author: Song Guo Zheng, 2011 Zonal Ave. HMR 710A, Los Angeles, CA 90033, USA. Tel: 323 442 2128; Fax: 323 442 2874; E-mail: szheng@usc.edu.
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suppressor/regulatory T cells, cytokine, Foxp3, autoimmunity |
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It has been well recognized that TGF-β is able to induce CD4+CD25+Foxp3+ suppressor/regulatory T (iTreg) cells and IL-2 facilitates iTreg induction and expansion, however, only half of TGF-β-induced CD4+CD25+ cells express Foxp3 and remaining CD4+CD25+Foxp3- cells may represent effector cells. Whether other factor(s) can increase Foxp3 expression by CD4+CD25+ cells induced with TGF-β is still unclear. Here we show that addition of exogenous IFN-γ or IL-4 diminished the ability of TGF-β to induce Foxp3 expression and IL-2 failed to rescue this decreased Foxp3 expression. Conversely, neutralization of IFN-γ and IL-4 significantly enhanced the ability of TGF-β to induce Foxp3 and develop the suppressive activity, indicating that different cytokine profiles affect the differentiation of CD4+CD25+Foxp3+ subset induced by TGF-β. These results show that combination of antibodies against IFN-γ and IL-4 and TGF-β enhances the efficacy of generation and function of iTreg cells and may therefore provide a novel therapeutic strategy for the treatment of autoimmune and other chronic inflammatory diseases.
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