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Expression of TNFR2 defines a maximally suppressive subset of mouse CD4(+)CD25(+)FoxP3(+) T regulatory cells: Applicability to tumor-infiltrating T regulatory cells

  1. Author:
    Chen, X.
    Subleski, J. J.
    Kopf, H.
    Howard, O.
    Mannel, D. N.
    Oppenheim, J. J.

  2. Author Address

    Chen, Xin] NCI, Basic Res Program, SAIC Frederick Inc, Mol Immunoregulat Lab,Canc Inflammat Program, Frederick, MD 21702 USA. [Kopf, Heather, Howard, O. M. Zack, Oppenheim, Joost J.] NCI, Canc Inflammat Program, Ctr Canc Res, Mol Immunoregulat Lab, Frederick, MD 21702 USA. [Subleski, Jeffrey J.] NCI, Expt Immunol Lab, Ctr Canc Res, Frederick, MD 21702 USA. [Maennel, Daniela N.] Univ Regensburg, Inst Immunol, Regensburg, Germany.
    1. Year: 2008
  2. Journal: Journal of Immunology
    1. 180
    2. 10
    3. Pages: 6467-6471
  4. Type of Article: Article
  1. Abstract:

    TNFR2 is predominantly expressed by a subset of human and mouse CD4(+)CD25A(+)FoxP3(+) T regulatory cells (Tregs). In this study, we characterized the phenotype and function of TNFR2(+) Tregs in peripheral lymphoid tissues Of normal and tumor-bearing C57BL/6 mice. We found that TNFR2 was expressed on 30-40% of the Tregs of the peripheral activated/memory subset that were most highly suppressive. In contrast, TNFR2(-) Tregs exhibited the phenotype of naive cells and only bad minimal suppressive activity. Although not typically considered to be Tregs, CD4(+) CD25(-) TNFR2(+) cells nevertheless possessed moderate suppressive activity. Strikingly, the suppressive activity of TNFR2(+) Tregs was considerably more potent than that of reportedly highly suppressive CD103(+) Tregs. In the Lewis lung carcinoma model, more highly suppressive TNFR2(+) Tregs accumulated intratumorally than in the periphery. Thus, TNFR2 identifies a unique subset of mouse Tregs with an activated/memory phenotype and maximal suppressive activity that may account for tumor-infiltrating lymphocyte-mediated immune evasion by tumors.

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External Sources

  1. PMID: 18453563

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