Skip NavigationSkip to Content

The phenotypic and functional consequences of tumour necrosis factor receptor type 2 expression on CD4(+) FoxP3(+) regulatory T cells

  1. Author:
    Chen, X.
    Oppenheim, J. J.
  2. Author Address

    [Chen, X] NCI, BSP, SAIC Frederick Inc, Lab Mol Immunoregulat,Canc Inflammat Program,Ctr, Frederick, MD 21702 USA;Chen, X (reprint author), NCI, BSP, SAIC Frederick Inc, Lab Mol Immunoregulat,Canc Inflammat Program,Ctr, POB B,Bldg 560,Rm 31-19, Frederick, MD 21702 USA;chenxin@mail.nih.gov oppenhej@mail.nih.gov
    1. Year: 2011
    2. Date: Aug
  1. Journal: Immunology
    1. 133
    2. 4
    3. Pages: 426-433
  2. Type of Article: Review
  3. ISSN: 0019-2805
  1. Abstract:

    Cytokine receptors expressed by CD4(+) FoxP3(+) regulatory T cells (Treg cells) not only serve as a phenotypic marker for the identification of this important population of immunosuppressive cells, they also promote the function of Treg cells. CD25, the alpha-chain of interleukin-2 receptor, is a prototype of such a receptor, which enables Treg cells to be activated by interleukin-2. We and others have found that tumour necrosis factor receptor type 2 (TNFR2) is another important cytokine receptor preferentially expressed by Treg cells with important phenotypic and functional roles. TNFR2 is preferentially expressed by highly functional human and mouse Treg cells, and mediates the activating effect of TNF on Treg cells. We review here the studies of the regulation of expression of TNFR2 on functional Treg cells as well as on CD4(+) FoxP3(-) effector T cells (Teff cells). We document the critical role of this receptor in the activation, proliferative expansion and survival of Treg cells. The contribution of TNFR2 expression on Treg and Teff cells to the beneficial and detrimental effects of anti-TNF treatment in autoimmune disorders will also be discussed.

    See More

External Sources

  1. DOI: 10.1111/j.1365-2567.2011.03460.x
  2. WOS: 000292332100004

Library Notes

  1. Fiscal Year: FY2010-2011
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel