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    Biochem Biophys Res Commun. 2007 Oct 12;362(1):44-50. Epub 2007 Aug 10.

    Functional and genomic analyses of FOXP3-transduced Jurkat-T cells as regulatory T (Treg)-like cells.

    Kim JY, Kim HJ, Hurt EM, Chen X, Howard OM, Farrar WL.

    Source

    Cancer Stem Cell Section, Laboratory of Cancer Prevention, NCI-Frederick, 1050 Boyles Street, Building 560, Room 21-78, Frederick, MD 21702, USA. jykim@ncifcrf.gov

    Abstract

    FOXP3, a forkhead transcription factor is essential for the development and function of CD4(+)CD25(+) regulatory T cells (Tregs). In contrast to conversion of murine naive T cells to Tregs by transduction of Foxp3, it is controversial whether ectopic expression of FOXP3 in human CD4(+) T cells is sufficient for acquisition of suppressive activity. Here, we show that retroviral transduction of FOXP3 induces a Treg phenotype in human leukemic CD4(+) Jurkat-T cells, evidenced by increased expression of Treg-associated cell surface markers as well as inhibition of cytokine production. Furthermore, FOXP3-transduced Jurkat-T cells suppress the proliferation of human CD4(+)CD25(-) T cells. Additionally, DNA microarray analysis identifies Treg-related genes regulated by FOXP3. Our study demonstrates that enforced expression of FOXP3 confers Treg-like properties on Jurkat-T cells, which can be a convenient and efficient Treg-like cell model for further study to identify Treg cell surface markers and target genes regulated by FOXP3.

    PMID:
    17706604
    [PubMed - indexed for MEDLINE]

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