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IL-2 induces in vivo suppression by CD4(+)CD25(+)Foxp3(+) regulatory T cells.
Eur J Immunol 2008; 38(6):1643-53EJ

Abstract

Interleukin-2 (IL-2) treatment is currently used to enhance T cell-mediated immune responses against tumors or in viral infections. At the same time, IL-2 is essential for the peripheral homeostasis of CD4(+)CD25(+)Foxp3(+)regulatory T cells (Treg). In our study, we show that IL-2 is also an important activator of Treg suppressive activity in vivo. IL-2 treatment induces Treg expansion as well as IL-10 production and increases their suppressive potential in vitro. Importantly, in vivo application of IL-2 via gene-gun vaccination using IL-2 encoding DNA plasmids (pIL-2) inhibited naive antigen-specific T cell proliferation as well as a Th1-induced delayed type hypersensitivity response. The suppressive effect can be transferred onto naive animals by Treg from IL-2-treated mice and the suppression depends on the synergistic action of IL-10 and TGF-beta. These data highlight that during therapeutic treatment with IL-2 the concomitant activation of Treg may indeed counteract the intended activation of cellular immunity.

Authors+Show Affiliations

Immunomodulation Group, Deutsches Rheuma-Forschungszentrum Berlin, Berlin, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18493984

Citation

Brandenburg, Susan, et al. "IL-2 Induces in Vivo Suppression By CD4(+)CD25(+)Foxp3(+) Regulatory T Cells." European Journal of Immunology, vol. 38, no. 6, 2008, pp. 1643-53.
Brandenburg S, Takahashi T, de la Rosa M, et al. IL-2 induces in vivo suppression by CD4(+)CD25(+)Foxp3(+) regulatory T cells. Eur J Immunol. 2008;38(6):1643-53.
Brandenburg, S., Takahashi, T., de la Rosa, M., Janke, M., Karsten, G., Muzzulini, T., ... Scheffold, A. (2008). IL-2 induces in vivo suppression by CD4(+)CD25(+)Foxp3(+) regulatory T cells. European Journal of Immunology, 38(6), pp. 1643-53. doi:10.1002/eji.200737791.
Brandenburg S, et al. IL-2 Induces in Vivo Suppression By CD4(+)CD25(+)Foxp3(+) Regulatory T Cells. Eur J Immunol. 2008;38(6):1643-53. PubMed PMID: 18493984.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - IL-2 induces in vivo suppression by CD4(+)CD25(+)Foxp3(+) regulatory T cells. AU - Brandenburg,Susan, AU - Takahashi,Takeshi, AU - de la Rosa,Maurus, AU - Janke,Marko, AU - Karsten,Gabriele, AU - Muzzulini,Till, AU - Orinska,Zane, AU - Bulfone-Paus,Silvia, AU - Scheffold,Alexander, PY - 2008/5/22/pubmed PY - 2008/8/19/medline PY - 2008/5/22/entrez SP - 1643 EP - 53 JF - European journal of immunology JO - Eur. J. Immunol. VL - 38 IS - 6 N2 - Interleukin-2 (IL-2) treatment is currently used to enhance T cell-mediated immune responses against tumors or in viral infections. At the same time, IL-2 is essential for the peripheral homeostasis of CD4(+)CD25(+)Foxp3(+)regulatory T cells (Treg). In our study, we show that IL-2 is also an important activator of Treg suppressive activity in vivo. IL-2 treatment induces Treg expansion as well as IL-10 production and increases their suppressive potential in vitro. Importantly, in vivo application of IL-2 via gene-gun vaccination using IL-2 encoding DNA plasmids (pIL-2) inhibited naive antigen-specific T cell proliferation as well as a Th1-induced delayed type hypersensitivity response. The suppressive effect can be transferred onto naive animals by Treg from IL-2-treated mice and the suppression depends on the synergistic action of IL-10 and TGF-beta. These data highlight that during therapeutic treatment with IL-2 the concomitant activation of Treg may indeed counteract the intended activation of cellular immunity. SN - 0014-2980 UR - https://www.unboundmedicine.com/medline/citation/18493984/IL_2_induces_in_vivo_suppression_by_CD4_+_CD25_+_Foxp3_+__regulatory_T_cells_ L2 - https://doi.org/10.1002/eji.200737791 DB - PRIME DP - Unbound Medicine ER -