Neutralization of IL-4 and IFN-γ Facilitates inducing TGF-β-induced CD4+Foxp3+ Regulatory Cells
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. Wheth...
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pubmed-36146702013-05-01 Neutralization of IL-4 and IFN-γ Facilitates inducing TGF-β-induced CD4+Foxp3+ Regulatory Cells Tao, Xiaojuan Ma, Jilin Zhang, Yonghua Yu, Jianning Cai, Long Wang, Juhua Zheng, Song Guo Article 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. Master Publishing Group 2008-03 /pmc/articles/PMC3614670/ /pubmed/23675066 Text en © Xiaojuan Tao et al. Licensee Master Publishing Group http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Tao, Xiaojuan Ma, Jilin Zhang, Yonghua Yu, Jianning Cai, Long Wang, Juhua Zheng, Song Guo |
spellingShingle |
Tao, Xiaojuan Ma, Jilin Zhang, Yonghua Yu, Jianning Cai, Long Wang, Juhua Zheng, Song Guo Neutralization of IL-4 and IFN-γ Facilitates inducing TGF-β-induced CD4+Foxp3+ Regulatory Cells |
author_facet |
Tao, Xiaojuan Ma, Jilin Zhang, Yonghua Yu, Jianning Cai, Long Wang, Juhua Zheng, Song Guo |
author_sort |
Tao, Xiaojuan |
title |
Neutralization of IL-4 and IFN-γ Facilitates inducing TGF-β-induced CD4+Foxp3+ Regulatory Cells |
title_short |
Neutralization of IL-4 and IFN-γ Facilitates inducing TGF-β-induced CD4+Foxp3+ Regulatory Cells |
title_full |
Neutralization of IL-4 and IFN-γ Facilitates inducing TGF-β-induced CD4+Foxp3+ Regulatory Cells |
title_fullStr |
Neutralization of IL-4 and IFN-γ Facilitates inducing TGF-β-induced CD4+Foxp3+ Regulatory Cells |
title_full_unstemmed |
Neutralization of IL-4 and IFN-γ Facilitates inducing TGF-β-induced CD4+Foxp3+ Regulatory Cells |
title_sort |
neutralization of il-4 and ifn-γ facilitates inducing tgf-β-induced cd4+foxp3+ regulatory cells |
description |
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. |
publisher |
Master Publishing Group |
publishDate |
2008 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3614670/ |
_version_ |
1611966991473573888 |