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P38 MAP kinase signaling is required for the conversion of CD4+CD25- T cells into iTreg.

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P38 MAP kinase signaling is required for the conversion of CD4+CD25- T cells into iTreg. / Huber, Samuel; Schrader, Jörg; Fritz, Gerhard; Presser, Katrin; Schmitt, Steffen; Waisman, Ari; Lüth, Stefan; Blessing, Manfred; Herkel, Johannes; Schramm, Christoph.

In: PLOS ONE, Vol. 3, No. 10, 10, 2008, p. 3302.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Huber, S, Schrader, J, Fritz, G, Presser, K, Schmitt, S, Waisman, A, Lüth, S, Blessing, M, Herkel, J & Schramm, C 2008, 'P38 MAP kinase signaling is required for the conversion of CD4+CD25- T cells into iTreg.', PLOS ONE, vol. 3, no. 10, 10, pp. 3302. https://doi.org/10.1371/journal.pone.0003302

APA

Huber, S., Schrader, J., Fritz, G., Presser, K., Schmitt, S., Waisman, A., Lüth, S., Blessing, M., Herkel, J., & Schramm, C. (2008). P38 MAP kinase signaling is required for the conversion of CD4+CD25- T cells into iTreg. PLOS ONE, 3(10), 3302. [10]. https://doi.org/10.1371/journal.pone.0003302

Vancouver

Huber S, Schrader J, Fritz G, Presser K, Schmitt S, Waisman A et al. P38 MAP kinase signaling is required for the conversion of CD4+CD25- T cells into iTreg. PLOS ONE. 2008;3(10):3302. 10. https://doi.org/10.1371/journal.pone.0003302

Bibtex

@article{51d99713e0ee4fb3b583a726e5e2a663,
title = "P38 MAP kinase signaling is required for the conversion of CD4+CD25- T cells into iTreg.",
abstract = "CD4+CD25+ regulatory T cells (Treg) are important mediators of immune tolerance. A subset of Treg can be generated in the periphery by TGF-beta dependent conversion of conventional CD4+CD25- T cells into induced Treg (iTreg). In chronic viral infection or malignancy, such induced iTreg, which limit the depletion of aberrant or infected cells, may be of pathogenic relevance. To identify potential targets for therapeutic intervention, we investigated the TGF-beta signaling in Treg. In contrast to conventional CD4+ T cells, Treg exhibited marked activation of the p38 MAP kinase pathway. Inhibition of p38 MAP kinase activity prevented the TGF-beta-dependent conversion of CD4+CD25- T cells into Foxp3+ iTreg in vitro. Of note, the suppressive capacity of nTreg was not affected by inhibiting p38 MAP kinase. Our findings indicate that signaling via p38 MAP kinase seems to be important for the peripheral generation of iTreg; p38 MAP kinase could thus be a therapeutic target to enhance immunity to chronic viral infection or cancer.",
author = "Samuel Huber and J{\"o}rg Schrader and Gerhard Fritz and Katrin Presser and Steffen Schmitt and Ari Waisman and Stefan L{\"u}th and Manfred Blessing and Johannes Herkel and Christoph Schramm",
year = "2008",
doi = "10.1371/journal.pone.0003302",
language = "Deutsch",
volume = "3",
pages = "3302",
journal = "PLOS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "10",

}

RIS

TY - JOUR

T1 - P38 MAP kinase signaling is required for the conversion of CD4+CD25- T cells into iTreg.

AU - Huber, Samuel

AU - Schrader, Jörg

AU - Fritz, Gerhard

AU - Presser, Katrin

AU - Schmitt, Steffen

AU - Waisman, Ari

AU - Lüth, Stefan

AU - Blessing, Manfred

AU - Herkel, Johannes

AU - Schramm, Christoph

PY - 2008

Y1 - 2008

N2 - CD4+CD25+ regulatory T cells (Treg) are important mediators of immune tolerance. A subset of Treg can be generated in the periphery by TGF-beta dependent conversion of conventional CD4+CD25- T cells into induced Treg (iTreg). In chronic viral infection or malignancy, such induced iTreg, which limit the depletion of aberrant or infected cells, may be of pathogenic relevance. To identify potential targets for therapeutic intervention, we investigated the TGF-beta signaling in Treg. In contrast to conventional CD4+ T cells, Treg exhibited marked activation of the p38 MAP kinase pathway. Inhibition of p38 MAP kinase activity prevented the TGF-beta-dependent conversion of CD4+CD25- T cells into Foxp3+ iTreg in vitro. Of note, the suppressive capacity of nTreg was not affected by inhibiting p38 MAP kinase. Our findings indicate that signaling via p38 MAP kinase seems to be important for the peripheral generation of iTreg; p38 MAP kinase could thus be a therapeutic target to enhance immunity to chronic viral infection or cancer.

AB - CD4+CD25+ regulatory T cells (Treg) are important mediators of immune tolerance. A subset of Treg can be generated in the periphery by TGF-beta dependent conversion of conventional CD4+CD25- T cells into induced Treg (iTreg). In chronic viral infection or malignancy, such induced iTreg, which limit the depletion of aberrant or infected cells, may be of pathogenic relevance. To identify potential targets for therapeutic intervention, we investigated the TGF-beta signaling in Treg. In contrast to conventional CD4+ T cells, Treg exhibited marked activation of the p38 MAP kinase pathway. Inhibition of p38 MAP kinase activity prevented the TGF-beta-dependent conversion of CD4+CD25- T cells into Foxp3+ iTreg in vitro. Of note, the suppressive capacity of nTreg was not affected by inhibiting p38 MAP kinase. Our findings indicate that signaling via p38 MAP kinase seems to be important for the peripheral generation of iTreg; p38 MAP kinase could thus be a therapeutic target to enhance immunity to chronic viral infection or cancer.

U2 - 10.1371/journal.pone.0003302

DO - 10.1371/journal.pone.0003302

M3 - SCORING: Zeitschriftenaufsatz

VL - 3

SP - 3302

JO - PLOS ONE

JF - PLOS ONE

SN - 1932-6203

IS - 10

M1 - 10

ER -