TGF-β affects development and differentiation of human natural killer cell subsets

Authors

  • David S. J. Allan,

    1. Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA, USA
    2. Sunnybrook Research Institute, University of Toronto, Toronto, Ont., Canada
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    • These authors have contributed equally to this work.

  • Basya Rybalov,

    1. Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA, USA
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    • These authors have contributed equally to this work.

  • Génève Awong,

    1. Sunnybrook Research Institute, University of Toronto, Toronto, Ont., Canada
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  • Juan Carlos Zúñiga-Pflücker,

    1. Sunnybrook Research Institute, University of Toronto, Toronto, Ont., Canada
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  • Hernan D. Kopcow,

    1. Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA, USA
    Current affiliation:
    1. Division of Molecular and Vascular Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, USA
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  • James R. Carlyle,

    1. Sunnybrook Research Institute, University of Toronto, Toronto, Ont., Canada
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  • Jack L. Strominger

    Corresponding author
    1. Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA, USA
    • Department of Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA Fax: +1-617-496-8351
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Abstract

Human peripheral blood NK cells may be divided into two main subsets: CD56brightCD16 and CD56dimCD16+. Since TGF-β is known to influence the development of many leukocyte lineages, its effects on NK cell differentiation either from human CD34+Lin hematopoietic progenitor/stem cells in vitro or from peripheral blood NK cells were investigated. TGF-β represses development of NK cells from CD34+ progenitors and inhibits differentiation of CD16+ NK cells. Moreover, TGF-β also results in conversion of a minor fraction of CD56brightCD16+ cells found in peripheral blood into CD56brightCD16 cells, highlighting a possible role of the former as a developmental intermediate and of TGF-β in influencing the genesis of NK subsets found in blood.

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