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Coexpression of TGF-beta1 and IL-10 enables regulatory T cells to completely suppress airway hyperreactivity

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Coexpression of TGF-beta1 and IL-10 enables regulatory T cells to completely suppress airway hyperreactivity. / Presser, Katrin; Schwinge, Dorothee; Wegmann, Michael; Huber, Samuel; Schmitt, Steffen; Quaas, Alexander; Maxeiner, Joachim H; Finotto, Susetta; Lohse, Ansgar W.; Blessing, Manfred; Schramm, Christoph.

in: J IMMUNOL, Jahrgang 181, Nr. 11, 11, 01.12.2008, S. 7751-7758.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Presser, K, Schwinge, D, Wegmann, M, Huber, S, Schmitt, S, Quaas, A, Maxeiner, JH, Finotto, S, Lohse, AW, Blessing, M & Schramm, C 2008, 'Coexpression of TGF-beta1 and IL-10 enables regulatory T cells to completely suppress airway hyperreactivity', J IMMUNOL, Jg. 181, Nr. 11, 11, S. 7751-7758. https://doi.org/10.4049/jimmunol.181.11.7751

APA

Presser, K., Schwinge, D., Wegmann, M., Huber, S., Schmitt, S., Quaas, A., Maxeiner, J. H., Finotto, S., Lohse, A. W., Blessing, M., & Schramm, C. (2008). Coexpression of TGF-beta1 and IL-10 enables regulatory T cells to completely suppress airway hyperreactivity. J IMMUNOL, 181(11), 7751-7758. [11]. https://doi.org/10.4049/jimmunol.181.11.7751

Vancouver

Presser K, Schwinge D, Wegmann M, Huber S, Schmitt S, Quaas A et al. Coexpression of TGF-beta1 and IL-10 enables regulatory T cells to completely suppress airway hyperreactivity. J IMMUNOL. 2008 Dez 1;181(11):7751-7758. 11. https://doi.org/10.4049/jimmunol.181.11.7751

Bibtex

@article{1368ccf1c34345aabbeba7f0a4470e0e,
title = "Coexpression of TGF-beta1 and IL-10 enables regulatory T cells to completely suppress airway hyperreactivity",
abstract = "In allergic airway disease, Treg may play an important role in the modulation of airway hyperreactivity (AHR) and inflammation. We therefore investigated the therapeutic potential of Treg in an Ag-dependent murine asthma model. We here describe that AHR can be completely suppressed by adoptive transfer of Treg overexpressing active TGF-beta1. Using mice with impaired TGF-beta signaling in T cells, we could demonstrate that TGF-beta signaling in recipient effector T cells or transferred Treg themselves is not required for the protective effects on AHR. However, the expression of IL-10 by Treg was found to be essential for the suppression of AHR, since Treg overexpressing active TGF-beta1 but deficient in IL-10 lacked protective effects. Airway inflammation could not be significantly suppressed by wild-type or transgenic Treg. In conclusion, modulation of cytokine expression by Treg may have therapeutic potential for the treatment of AHR in asthma. The mechanisms of the effects of Treg on airway inflammation require further clarification.",
keywords = "Adoptive Transfer, Animals, Disease Models, Animal, Gene Expression, Inflammation, Interleukin-10, Mice, Mice, Transgenic, Respiratory Hypersensitivity, Signal Transduction, T-Lymphocytes, Regulatory, Transforming Growth Factor beta1, Journal Article, Research Support, Non-U.S. Gov't",
author = "Katrin Presser and Dorothee Schwinge and Michael Wegmann and Samuel Huber and Steffen Schmitt and Alexander Quaas and Maxeiner, {Joachim H} and Susetta Finotto and Lohse, {Ansgar W.} and Manfred Blessing and Christoph Schramm",
year = "2008",
month = dec,
day = "1",
doi = "10.4049/jimmunol.181.11.7751",
language = "English",
volume = "181",
pages = "7751--7758",
journal = "J IMMUNOL",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "11",

}

RIS

TY - JOUR

T1 - Coexpression of TGF-beta1 and IL-10 enables regulatory T cells to completely suppress airway hyperreactivity

AU - Presser, Katrin

AU - Schwinge, Dorothee

AU - Wegmann, Michael

AU - Huber, Samuel

AU - Schmitt, Steffen

AU - Quaas, Alexander

AU - Maxeiner, Joachim H

AU - Finotto, Susetta

AU - Lohse, Ansgar W.

AU - Blessing, Manfred

AU - Schramm, Christoph

PY - 2008/12/1

Y1 - 2008/12/1

N2 - In allergic airway disease, Treg may play an important role in the modulation of airway hyperreactivity (AHR) and inflammation. We therefore investigated the therapeutic potential of Treg in an Ag-dependent murine asthma model. We here describe that AHR can be completely suppressed by adoptive transfer of Treg overexpressing active TGF-beta1. Using mice with impaired TGF-beta signaling in T cells, we could demonstrate that TGF-beta signaling in recipient effector T cells or transferred Treg themselves is not required for the protective effects on AHR. However, the expression of IL-10 by Treg was found to be essential for the suppression of AHR, since Treg overexpressing active TGF-beta1 but deficient in IL-10 lacked protective effects. Airway inflammation could not be significantly suppressed by wild-type or transgenic Treg. In conclusion, modulation of cytokine expression by Treg may have therapeutic potential for the treatment of AHR in asthma. The mechanisms of the effects of Treg on airway inflammation require further clarification.

AB - In allergic airway disease, Treg may play an important role in the modulation of airway hyperreactivity (AHR) and inflammation. We therefore investigated the therapeutic potential of Treg in an Ag-dependent murine asthma model. We here describe that AHR can be completely suppressed by adoptive transfer of Treg overexpressing active TGF-beta1. Using mice with impaired TGF-beta signaling in T cells, we could demonstrate that TGF-beta signaling in recipient effector T cells or transferred Treg themselves is not required for the protective effects on AHR. However, the expression of IL-10 by Treg was found to be essential for the suppression of AHR, since Treg overexpressing active TGF-beta1 but deficient in IL-10 lacked protective effects. Airway inflammation could not be significantly suppressed by wild-type or transgenic Treg. In conclusion, modulation of cytokine expression by Treg may have therapeutic potential for the treatment of AHR in asthma. The mechanisms of the effects of Treg on airway inflammation require further clarification.

KW - Adoptive Transfer

KW - Animals

KW - Disease Models, Animal

KW - Gene Expression

KW - Inflammation

KW - Interleukin-10

KW - Mice

KW - Mice, Transgenic

KW - Respiratory Hypersensitivity

KW - Signal Transduction

KW - T-Lymphocytes, Regulatory

KW - Transforming Growth Factor beta1

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.4049/jimmunol.181.11.7751

DO - 10.4049/jimmunol.181.11.7751

M3 - SCORING: Journal article

C2 - 19017964

VL - 181

SP - 7751

EP - 7758

JO - J IMMUNOL

JF - J IMMUNOL

SN - 0022-1767

IS - 11

M1 - 11

ER -