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Blood, 15 October 2007, Vol. 110, No. 8, pp. 2983-2990. Prepublished online as a Blood First Edition Paper on July 20, 2007; DOI 10.1182/blood-2007-06-094656. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-06-094656v1 110/8/2983    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Tran, D. Q. Articles by Shevach, E. M. Search for Related Content PubMed PubMed Citation Articles by Tran, D. Q. Articles by Shevach, E. M. Related Collections Immunobiology Gene Expression Related Articles in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Induction of FOXP3 expression in naive human CD4+FOXP3– T cells by T-cell receptor stimulation is transforming growth factor-ß–dependent but does not confer a regulatory phenotype Dat Q. Tran1, Heather Ramsey1, and Ethan M. Shevach1 1 Laboratory of Immunology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD Thymic-derived natural T-regulatory cells (nTregs) are important for the induction of self-tolerance and the control of autoimmunity. Murine CD4+CD25–Foxp3– cells can be induced to express Foxp3 after T-cell receptor (TCR) activation in the presence of transforming growth factor ß (TGFß) and are phenotypically similar to nTregs. Some studies have suggested that TCR stimulation of human CD4+CD25– cells results in the induction of transient expression of FOXP3, but that the induced cells lack a regulatory phenotype. We demonstrate here that TCR stimulation alone was insufficient to induce FOXP3 expression in the absence of TGFß, whereas high levels of FOXP3 expression could be induced in the presence of TGFß. Although FOXP3 expression was stable, the TGFß-induced FOXP3+ T cells were neither anergic nor suppressive and produced high levels of effector cytokines. These results suggest that even high levels of FOXP3 expression are insufficient to define a human CD4+ T cell as a T-regulatory cell. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Articles in Blood Online: Defense of the clone: antibody 259D effectively labels human FOXP3 in a variety of applications Bridget C. Fox, Paola A. Bignone, Philip J. Brown, and Alison H. Banham Blood 2008 111: 3897-3899. [Full Text] [PDF] Attack on the clones? Human FOXP3 detection by PCH101, 236A/E7, 206D, and 259D reveals 259D as the outlier with lower sensitivity Vinodh Pillai and Nitin J. Karandikar Blood 2008 111: 463-464. [Full Text] [PDF] This article has been cited by other articles: B. Kavanagh, S. O'Brien, D. Lee, Y. Hou, V. Weinberg, B. Rini, J. P. Allison, E. J. Small, and L. Fong CTLA4 blockade expands FoxP3+ regulatory and activated effector CD4+ T cells in a dose-dependent fashion Blood, August 15, 2008; 112(4): 1175 - 1183. [Abstract] [Full Text] [PDF] E. S. Yolcu, X. Gu, C. Lacelle, H. Zhao, L. Bandura-Morgan, N. Askenasy, and H. Shirwan Induction of Tolerance to Cardiac Allografts Using Donor Splenocytes Engineered to Display on Their Surface an Exogenous Fas Ligand Protein J. Immunol., July 15, 2008; 181(2): 931 - 939. [Abstract] [Full Text] [PDF] C. Scotta, M. Soligo, C. Camperio, and E. 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