Research ExplorerPublicationsCutting edge: TGF-beta signaling is required for the in vivo...

Cutting edge: TGF-beta signaling is required for the in vivo expansion and immunosuppressive capacity of regulatory CD4+CD25+ T cells

Standard

Cutting edge: TGF-beta signaling is required for the in vivo expansion and immunosuppressive capacity of regulatory CD4+CD25+ T cells. / Huber, Samuel; Schramm, Christoph; Lehr, Hans A; Mann, Amrit; Schmitt, Steffen; Becker, Christoph; Protschka, Martina; Galle, Peter R; Neurath, Markus F; Blessing, Manfred.

In: J IMMUNOL, Vol. 173, No. 11, 01.12.2004, p. 6526-31.

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

Harvard

Huber, S, Schramm, C, Lehr, HA, Mann, A, Schmitt, S, Becker, C, Protschka, M, Galle, PR, Neurath, MF & Blessing, M 2004, 'Cutting edge: TGF-beta signaling is required for the in vivo expansion and immunosuppressive capacity of regulatory CD4+CD25+ T cells', J IMMUNOL, vol. 173, no. 11, pp. 6526-31. https://doi.org/10.4049/jimmunol.173.11.6526

APA

Huber, S., Schramm, C., Lehr, H. A., Mann, A., Schmitt, S., Becker, C., Protschka, M., Galle, P. R., Neurath, M. F., & Blessing, M. (2004). Cutting edge: TGF-beta signaling is required for the in vivo expansion and immunosuppressive capacity of regulatory CD4+CD25+ T cells. J IMMUNOL, 173(11), 6526-31. https://doi.org/10.4049/jimmunol.173.11.6526

Vancouver

Huber S, Schramm C, Lehr HA, Mann A, Schmitt S, Becker C et al. Cutting edge: TGF-beta signaling is required for the in vivo expansion and immunosuppressive capacity of regulatory CD4+CD25+ T cells. J IMMUNOL. 2004 Dec 1;173(11):6526-31. https://doi.org/10.4049/jimmunol.173.11.6526

Bibtex

@article{284884b4d6d14f7b98ca93f19f81f28f,
title = "Cutting edge: TGF-beta signaling is required for the in vivo expansion and immunosuppressive capacity of regulatory CD4+CD25+ T cells",
abstract = "Data regarding the role of TGF-beta for the in vivo function of regulatory CD4(+)CD25(+) T cells (Treg) are controversial. A transgenic mouse model with impaired TGF-beta signaling specifically in T cells was used to assess the role of endogenous TGF-beta for the in vivo function of CD4(+)CD25(+) Treg in a murine model of colitis induced by dextran sulfate. Transfer of wild-type, but not transgenic CD4(+)CD25(+) Treg was found to suppress colitis in wild-type mice. In addition, by transferring CFSE-labeled CD4(+)CD25(+) Treg we could demonstrate that endogenous TGF-beta promotes the expansion of CD4(+)CD25(+) Treg in vivo. Transgenic mice themselves developed reduced numbers of peripheral CD4(+)CD25(+) Treg and were more susceptible to the induction of colitis, which could be prevented by the transfer of wild-type Treg. These data indicate that TGF-beta signaling in CD4(+)CD25(+) Treg is required for their in vivo expansion and suppressive capacity.",
keywords = "Adoptive Transfer, Animals, Cell Differentiation/genetics, Colitis/genetics, Genetic Predisposition to Disease, Humans, Lymphocyte Count, Mice, Receptors, Interleukin-2/biosynthesis, Signal Transduction/genetics, T-Lymphocytes, Regulatory/cytology, Transforming Growth Factor beta/physiology",
author = "Samuel Huber and Christoph Schramm and Lehr, {Hans A} and Amrit Mann and Steffen Schmitt and Christoph Becker and Martina Protschka and Galle, {Peter R} and Neurath, {Markus F} and Manfred Blessing",
year = "2004",
month = dec,
day = "1",
doi = "10.4049/jimmunol.173.11.6526",
language = "English",
volume = "173",
pages = "6526--31",
journal = "J IMMUNOL",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "11",

}

RIS

TY - JOUR

T1 - Cutting edge: TGF-beta signaling is required for the in vivo expansion and immunosuppressive capacity of regulatory CD4+CD25+ T cells

AU - Huber, Samuel

AU - Schramm, Christoph

AU - Lehr, Hans A

AU - Mann, Amrit

AU - Schmitt, Steffen

AU - Becker, Christoph

AU - Protschka, Martina

AU - Galle, Peter R

AU - Neurath, Markus F

AU - Blessing, Manfred

PY - 2004/12/1

Y1 - 2004/12/1

N2 - Data regarding the role of TGF-beta for the in vivo function of regulatory CD4(+)CD25(+) T cells (Treg) are controversial. A transgenic mouse model with impaired TGF-beta signaling specifically in T cells was used to assess the role of endogenous TGF-beta for the in vivo function of CD4(+)CD25(+) Treg in a murine model of colitis induced by dextran sulfate. Transfer of wild-type, but not transgenic CD4(+)CD25(+) Treg was found to suppress colitis in wild-type mice. In addition, by transferring CFSE-labeled CD4(+)CD25(+) Treg we could demonstrate that endogenous TGF-beta promotes the expansion of CD4(+)CD25(+) Treg in vivo. Transgenic mice themselves developed reduced numbers of peripheral CD4(+)CD25(+) Treg and were more susceptible to the induction of colitis, which could be prevented by the transfer of wild-type Treg. These data indicate that TGF-beta signaling in CD4(+)CD25(+) Treg is required for their in vivo expansion and suppressive capacity.

AB - Data regarding the role of TGF-beta for the in vivo function of regulatory CD4(+)CD25(+) T cells (Treg) are controversial. A transgenic mouse model with impaired TGF-beta signaling specifically in T cells was used to assess the role of endogenous TGF-beta for the in vivo function of CD4(+)CD25(+) Treg in a murine model of colitis induced by dextran sulfate. Transfer of wild-type, but not transgenic CD4(+)CD25(+) Treg was found to suppress colitis in wild-type mice. In addition, by transferring CFSE-labeled CD4(+)CD25(+) Treg we could demonstrate that endogenous TGF-beta promotes the expansion of CD4(+)CD25(+) Treg in vivo. Transgenic mice themselves developed reduced numbers of peripheral CD4(+)CD25(+) Treg and were more susceptible to the induction of colitis, which could be prevented by the transfer of wild-type Treg. These data indicate that TGF-beta signaling in CD4(+)CD25(+) Treg is required for their in vivo expansion and suppressive capacity.

KW - Adoptive Transfer

KW - Animals

KW - Cell Differentiation/genetics

KW - Colitis/genetics

KW - Genetic Predisposition to Disease

KW - Humans

KW - Lymphocyte Count

KW - Mice

KW - Receptors, Interleukin-2/biosynthesis

KW - Signal Transduction/genetics

KW - T-Lymphocytes, Regulatory/cytology

KW - Transforming Growth Factor beta/physiology

U2 - 10.4049/jimmunol.173.11.6526

DO - 10.4049/jimmunol.173.11.6526

M3 - SCORING: Journal article

C2 - 15557141

VL - 173

SP - 6526

EP - 6531

JO - J IMMUNOL

JF - J IMMUNOL

SN - 0022-1767

IS - 11

ER -