Rhoh deficiency reduces peripheral T-cell function and attenuates allogenic transplant rejection

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Rhoh deficiency reduces peripheral T-cell function and attenuates allogenic transplant rejection. / Porubsky, Stefan; Wang, Shijun; Kiss, Eva; Dehmel, Stefan; Bonrouhi, Mahnaz; Dorn, Tatjana; Luckow, Bruno; Brakebusch, Cord; Gröne, Hermann-Josef.

I: European Journal of Immunology, Bind 41, Nr. 1, 01.01.2011, s. 76-88.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Porubsky, S, Wang, S, Kiss, E, Dehmel, S, Bonrouhi, M, Dorn, T, Luckow, B, Brakebusch, C & Gröne, H-J 2011, 'Rhoh deficiency reduces peripheral T-cell function and attenuates allogenic transplant rejection', European Journal of Immunology, bind 41, nr. 1, s. 76-88. https://doi.org/10.1002/eji.201040420

APA

Porubsky, S., Wang, S., Kiss, E., Dehmel, S., Bonrouhi, M., Dorn, T., Luckow, B., Brakebusch, C., & Gröne, H-J. (2011). Rhoh deficiency reduces peripheral T-cell function and attenuates allogenic transplant rejection. European Journal of Immunology, 41(1), 76-88. https://doi.org/10.1002/eji.201040420

Vancouver

Porubsky S, Wang S, Kiss E, Dehmel S, Bonrouhi M, Dorn T o.a. Rhoh deficiency reduces peripheral T-cell function and attenuates allogenic transplant rejection. European Journal of Immunology. 2011 jan. 1;41(1):76-88. https://doi.org/10.1002/eji.201040420

Author

Porubsky, Stefan ; Wang, Shijun ; Kiss, Eva ; Dehmel, Stefan ; Bonrouhi, Mahnaz ; Dorn, Tatjana ; Luckow, Bruno ; Brakebusch, Cord ; Gröne, Hermann-Josef. / Rhoh deficiency reduces peripheral T-cell function and attenuates allogenic transplant rejection. I: European Journal of Immunology. 2011 ; Bind 41, Nr. 1. s. 76-88.

Bibtex

@article{94b66077a7ea4335bc317447fd137b54,
title = "Rhoh deficiency reduces peripheral T-cell function and attenuates allogenic transplant rejection",
abstract = "Rhoh is a hematopoietic system-specific GTPase. Rhoh-deficient T cells have been shown to have a defect in TCR signaling manifested during their thymic development. Our aims were to investigate the phenotype of peripheral Rhoh-deficient T cells and to explore in vivo the potential benefit of Rhoh deficiency in a clinically relevant situation, in which T-cell inhibition is desirable. In murine allogenic kidney transplantation, Rhoh deficiency caused a significant 75% reduction of acute and chronic transplant rejection accompanied by 75% lower alloantigen-specific antibody levels and significantly better graft function. This effect was independent of the lower T-cell numbers in Rhoh-deficient recipients, because injection of equal numbers of Rhoh-deficient or control T cells into kidney transplanted mice with SCID led again to a significant 60% reduction of rejection. Mixed lymphocyte reaction revealed that the weaker alloreactivity was associated with a 85% lower cytotoxicity and a 50-80% lower cytokine release in Rhoh-deficient T cells without an influence on the secretion itself. Antigen uptake and presentation in DC were unaffected by Rhoh deficiency. These findings stress the importance of Rhoh for the function of peripheral T cells.",
keywords = "Acute Disease, Animals, Antibodies, Antigen Presentation, Chronic Disease, Cytokines, Dendritic Cells, Graft Rejection, Isoantigens, Kidney Transplantation, Lymphocyte Culture Test, Mixed, Male, Mice, Mice, Inbred BALB C, Mice, Mutant Strains, Mice, SCID, T-Lymphocytes, Transcription Factors, rho GTP-Binding Proteins",
author = "Stefan Porubsky and Shijun Wang and Eva Kiss and Stefan Dehmel and Mahnaz Bonrouhi and Tatjana Dorn and Bruno Luckow and Cord Brakebusch and Hermann-Josef Gr{\"o}ne",
note = "Copyright {\textcopyright} 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.",
year = "2011",
month = jan,
day = "1",
doi = "10.1002/eji.201040420",
language = "English",
volume = "41",
pages = "76--88",
journal = "European Journal of Immunology",
issn = "0014-2980",
publisher = "Wiley - V C H Verlag GmbH & Co. KGaA",
number = "1",

}

RIS

TY - JOUR

T1 - Rhoh deficiency reduces peripheral T-cell function and attenuates allogenic transplant rejection

AU - Porubsky, Stefan

AU - Wang, Shijun

AU - Kiss, Eva

AU - Dehmel, Stefan

AU - Bonrouhi, Mahnaz

AU - Dorn, Tatjana

AU - Luckow, Bruno

AU - Brakebusch, Cord

AU - Gröne, Hermann-Josef

N1 - Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

PY - 2011/1/1

Y1 - 2011/1/1

N2 - Rhoh is a hematopoietic system-specific GTPase. Rhoh-deficient T cells have been shown to have a defect in TCR signaling manifested during their thymic development. Our aims were to investigate the phenotype of peripheral Rhoh-deficient T cells and to explore in vivo the potential benefit of Rhoh deficiency in a clinically relevant situation, in which T-cell inhibition is desirable. In murine allogenic kidney transplantation, Rhoh deficiency caused a significant 75% reduction of acute and chronic transplant rejection accompanied by 75% lower alloantigen-specific antibody levels and significantly better graft function. This effect was independent of the lower T-cell numbers in Rhoh-deficient recipients, because injection of equal numbers of Rhoh-deficient or control T cells into kidney transplanted mice with SCID led again to a significant 60% reduction of rejection. Mixed lymphocyte reaction revealed that the weaker alloreactivity was associated with a 85% lower cytotoxicity and a 50-80% lower cytokine release in Rhoh-deficient T cells without an influence on the secretion itself. Antigen uptake and presentation in DC were unaffected by Rhoh deficiency. These findings stress the importance of Rhoh for the function of peripheral T cells.

AB - Rhoh is a hematopoietic system-specific GTPase. Rhoh-deficient T cells have been shown to have a defect in TCR signaling manifested during their thymic development. Our aims were to investigate the phenotype of peripheral Rhoh-deficient T cells and to explore in vivo the potential benefit of Rhoh deficiency in a clinically relevant situation, in which T-cell inhibition is desirable. In murine allogenic kidney transplantation, Rhoh deficiency caused a significant 75% reduction of acute and chronic transplant rejection accompanied by 75% lower alloantigen-specific antibody levels and significantly better graft function. This effect was independent of the lower T-cell numbers in Rhoh-deficient recipients, because injection of equal numbers of Rhoh-deficient or control T cells into kidney transplanted mice with SCID led again to a significant 60% reduction of rejection. Mixed lymphocyte reaction revealed that the weaker alloreactivity was associated with a 85% lower cytotoxicity and a 50-80% lower cytokine release in Rhoh-deficient T cells without an influence on the secretion itself. Antigen uptake and presentation in DC were unaffected by Rhoh deficiency. These findings stress the importance of Rhoh for the function of peripheral T cells.

KW - Acute Disease

KW - Animals

KW - Antibodies

KW - Antigen Presentation

KW - Chronic Disease

KW - Cytokines

KW - Dendritic Cells

KW - Graft Rejection

KW - Isoantigens

KW - Kidney Transplantation

KW - Lymphocyte Culture Test, Mixed

KW - Male

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Mutant Strains

KW - Mice, SCID

KW - T-Lymphocytes

KW - Transcription Factors

KW - rho GTP-Binding Proteins

U2 - 10.1002/eji.201040420

DO - 10.1002/eji.201040420

M3 - Journal article

C2 - 21182079

VL - 41

SP - 76

EP - 88

JO - European Journal of Immunology

JF - European Journal of Immunology

SN - 0014-2980

IS - 1

ER -

ID: 33902024