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Expression of FOXP3 mRNA is not confined to CD4+CD25+ T regulatory cells in humans.
 
Diabetes OD > Development and Function of Pancreas and Immunity > Immune System > Activation and Inhibition > Regulatory Mechanisms > Treg cells > FoxP3 > FoxP3 Genes > Journal Article

(Journal Article): Expression of FOXP3 mRNA is not confined to CD4+CD25+ T regulatory cells in humans.
 
Morgan ME, van Bilsen JH, Bakker AM, Heemskerk B, Schilham MW, Hartgers FC, Elferink BG, van der Zanden L, de Vries RR, Huizinga TW (Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands., M.Morgan@ncmls.kun.nl )
 
IN: Hum Immunol 2005; 66(1):13-20
Impact Factor(s) of Hum Immunol: 2.664 (2004), 2.619 (2003), 2.573 (2002), 2.373 (2001)

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ABSTRACT: Expression of the transcription factor Foxp3 (forkhead box P3) has been implicated as a key element for CD25(+) T regulatory cell function in mice. However, literature over similar involvement of FOXP3 expression in human T regulatory cells is limited. We found that, unlike murine cells, FOXP3 mRNA expression could be induced in human CD25(-) and CD8(+) peripheral blood mononuclear cells, which were both negative for FOXP3 mRNA expression after isolation. Expression of FOXP3 mRNA began as soon as 24-40 hours after stimulation, demonstrating a correlation between activation and FOXP3 mRNA expression in human cells. In order to determine whether FOXP3 expression is confined to CD4(+)CD25(+) T cells with a regulatory phenotype, we analyzed several well-defined T-cell clones and lines with various specificities. Surprisingly, expression of FOXP3 mRNA was detected in all clones and limited to the CD25(hi) populations. Nonetheless, the CD25(hi) fraction did not display regulatory properties because both the CD25(hi) and CD25(low) populations exhibited a similar proliferative- and interferon-gamma-secreting potential after antigenic stimulation. These results indicate that FOXP3 expression in humans, unlike mice, may not be specific for cells with a regulatory phenotype and may be only a consequence of activation status.

TYPE OF PUBLICATION: Original article

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