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

  1. Author:
    Kim, J. Y.
    Kim, H. J.
    Hurt, E. M.
    Chen, X.
    Howard, O. M. Z.
    Farrar, W. L.

  2. Author Address

    NCI, Canc Stem Cell Sect, Lab Canc Prevent, Frederick, MD 21702 USA. SAIC Frederick Inc, Basic Res Program, Frederick, MD 21702 USA. Canc Res Ctr, Natl Canc Inst, Lab Mol Immunoregulat, Frederick, MD 21702 USA.;Farrar, WL, NCI, Canc Stem Cell Sect, Lab Canc Prevent, 1050 Boyles St, Frederick, MD 21702 USA.;jykim@ncifcrf.gov farrar@mail.ncifcrf.gov
    1. Year: 2007
    2. Date: Oct
  2. Journal: Biochemical and Biophysical Research Communications
    1. 362
    2. 1
    3. Pages: 44-50
  4. Type of Article: Article
  5. ISSN: 0006-291X
  1. 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 Treglike cell model for further study to identify Treg cell surface markers and target genes regulated by FOXP3. (c) 2007 Elsevier Inc. All rights reserved.

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External Sources

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  2. DOI: 10.1016/j.bbrc.2007.07.187
  3. View record in Web of Science®
  4. WOS: 000249357700008

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