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Susceptibility to collagen-induced arthritis is modulated by TGFbeta responsiveness of T cells

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Susceptibility to collagen-induced arthritis is modulated by TGFbeta responsiveness of T cells. / Schramm, Christoph; Kriegsmann, Jörg; Protschka, Martina; Huber, Samuel; Hansen, Torsten; Schmitt, Edgar; Galle, Peter Robert; Blessing, Manfred.

In: ARTHRITIS RES THER, Vol. 6, No. 2, 2004, p. R114-R119.

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

Harvard

Schramm, C, Kriegsmann, J, Protschka, M, Huber, S, Hansen, T, Schmitt, E, Galle, PR & Blessing, M 2004, 'Susceptibility to collagen-induced arthritis is modulated by TGFbeta responsiveness of T cells', ARTHRITIS RES THER, vol. 6, no. 2, pp. R114-R119. https://doi.org/10.1186/ar1039

APA

Schramm, C., Kriegsmann, J., Protschka, M., Huber, S., Hansen, T., Schmitt, E., Galle, P. R., & Blessing, M. (2004). Susceptibility to collagen-induced arthritis is modulated by TGFbeta responsiveness of T cells. ARTHRITIS RES THER, 6(2), R114-R119. https://doi.org/10.1186/ar1039

Vancouver

Schramm C, Kriegsmann J, Protschka M, Huber S, Hansen T, Schmitt E et al. Susceptibility to collagen-induced arthritis is modulated by TGFbeta responsiveness of T cells. ARTHRITIS RES THER. 2004;6(2):R114-R119. https://doi.org/10.1186/ar1039

Bibtex

@article{c1066b039ecb49b5b3e7c71294cb6f7d,
title = "Susceptibility to collagen-induced arthritis is modulated by TGFbeta responsiveness of T cells",
abstract = "The objective of our study was to determine the regulatory effects that endogenous transforming growth factor beta (TGFbeta) exerts on T cells in the pathogenesis of collagen-induced arthritis (CIA). CIA was induced in transgenic mice expressing a dominant negative TGFbeta type II receptor in T cells under the control of the human CD2 promoter. Clinical and histological arthritis scores were determined and experiments on disease induction and the healing phase of disease were performed. The proliferation and cytokine production of draining lymph node cells in vitro were analyzed. Transgenic mice were more susceptible to induction of CIA. The overall incidence was higher in transgenic mice than in wild-type mice (57% vs 35%, P < 0.05). Affected transgenic animals displayed a significantly higher clinical (4.5 +/- 0.6 vs 1.67 +/- 0.19, P = 0.001) and histological arthritis score (8.01 +/- 0.9 vs 4.06 +/- 1.1, P < 0.05). Draining lymph node cells of transgenic mice secreted more tumor necrosis factor alpha and IFNgamma and proliferated more vigorously in response to collagen type II and upon CD3/CD28 costimulation in vitro. Therefore, the regulation of T cells by endogenous TGFbeta is important for the maintenance of joint integrity after arthritis induction. Defects in TGFbeta-signalling as a susceptibility factor for rheumatoid arthritis may warrant further investigation.",
keywords = "Animals, Arthritis, Experimental/chemically induced, Arthritis, Rheumatoid/chemically induced, Cattle, Cell Proliferation, Cells, Cultured, Collagen Type II/immunology, Crosses, Genetic, Cytokines/biosynthesis, Disease Susceptibility, Lymph Nodes/pathology, Mice, Mice, Inbred DBA, Mice, Inbred Strains, Mice, Transgenic, Severity of Illness Index, T-Lymphocytes/physiology, Th1 Cells/metabolism, Transforming Growth Factor beta/physiology",
author = "Christoph Schramm and J{\"o}rg Kriegsmann and Martina Protschka and Samuel Huber and Torsten Hansen and Edgar Schmitt and Galle, {Peter Robert} and Manfred Blessing",
year = "2004",
doi = "10.1186/ar1039",
language = "English",
volume = "6",
pages = "R114--R119",
journal = "ARTHRITIS RES THER",
issn = "1478-6354",
publisher = "Springer",
number = "2",

}

RIS

TY - JOUR

T1 - Susceptibility to collagen-induced arthritis is modulated by TGFbeta responsiveness of T cells

AU - Schramm, Christoph

AU - Kriegsmann, Jörg

AU - Protschka, Martina

AU - Huber, Samuel

AU - Hansen, Torsten

AU - Schmitt, Edgar

AU - Galle, Peter Robert

AU - Blessing, Manfred

PY - 2004

Y1 - 2004

N2 - The objective of our study was to determine the regulatory effects that endogenous transforming growth factor beta (TGFbeta) exerts on T cells in the pathogenesis of collagen-induced arthritis (CIA). CIA was induced in transgenic mice expressing a dominant negative TGFbeta type II receptor in T cells under the control of the human CD2 promoter. Clinical and histological arthritis scores were determined and experiments on disease induction and the healing phase of disease were performed. The proliferation and cytokine production of draining lymph node cells in vitro were analyzed. Transgenic mice were more susceptible to induction of CIA. The overall incidence was higher in transgenic mice than in wild-type mice (57% vs 35%, P < 0.05). Affected transgenic animals displayed a significantly higher clinical (4.5 +/- 0.6 vs 1.67 +/- 0.19, P = 0.001) and histological arthritis score (8.01 +/- 0.9 vs 4.06 +/- 1.1, P < 0.05). Draining lymph node cells of transgenic mice secreted more tumor necrosis factor alpha and IFNgamma and proliferated more vigorously in response to collagen type II and upon CD3/CD28 costimulation in vitro. Therefore, the regulation of T cells by endogenous TGFbeta is important for the maintenance of joint integrity after arthritis induction. Defects in TGFbeta-signalling as a susceptibility factor for rheumatoid arthritis may warrant further investigation.

AB - The objective of our study was to determine the regulatory effects that endogenous transforming growth factor beta (TGFbeta) exerts on T cells in the pathogenesis of collagen-induced arthritis (CIA). CIA was induced in transgenic mice expressing a dominant negative TGFbeta type II receptor in T cells under the control of the human CD2 promoter. Clinical and histological arthritis scores were determined and experiments on disease induction and the healing phase of disease were performed. The proliferation and cytokine production of draining lymph node cells in vitro were analyzed. Transgenic mice were more susceptible to induction of CIA. The overall incidence was higher in transgenic mice than in wild-type mice (57% vs 35%, P < 0.05). Affected transgenic animals displayed a significantly higher clinical (4.5 +/- 0.6 vs 1.67 +/- 0.19, P = 0.001) and histological arthritis score (8.01 +/- 0.9 vs 4.06 +/- 1.1, P < 0.05). Draining lymph node cells of transgenic mice secreted more tumor necrosis factor alpha and IFNgamma and proliferated more vigorously in response to collagen type II and upon CD3/CD28 costimulation in vitro. Therefore, the regulation of T cells by endogenous TGFbeta is important for the maintenance of joint integrity after arthritis induction. Defects in TGFbeta-signalling as a susceptibility factor for rheumatoid arthritis may warrant further investigation.

KW - Animals

KW - Arthritis, Experimental/chemically induced

KW - Arthritis, Rheumatoid/chemically induced

KW - Cattle

KW - Cell Proliferation

KW - Cells, Cultured

KW - Collagen Type II/immunology

KW - Crosses, Genetic

KW - Cytokines/biosynthesis

KW - Disease Susceptibility

KW - Lymph Nodes/pathology

KW - Mice

KW - Mice, Inbred DBA

KW - Mice, Inbred Strains

KW - Mice, Transgenic

KW - Severity of Illness Index

KW - T-Lymphocytes/physiology

KW - Th1 Cells/metabolism

KW - Transforming Growth Factor beta/physiology

U2 - 10.1186/ar1039

DO - 10.1186/ar1039

M3 - SCORING: Journal article

C2 - 15059274

VL - 6

SP - R114-R119

JO - ARTHRITIS RES THER

JF - ARTHRITIS RES THER

SN - 1478-6354

IS - 2

ER -