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Chemokine receptor CXCR3 mediates T cell recruitment and tissue injury in nephrotoxic nephritis in mice.

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Chemokine receptor CXCR3 mediates T cell recruitment and tissue injury in nephrotoxic nephritis in mice. / Panzer, Ulf; Steinmetz, Oliver; Paust, Hans-Joachim; Meyer-Schwesinger, Catherine; Peters, Anett; Turner, Jan Eric; Zahner, Gunther; Heymann, Felix; Kurts, Christian; Hopfer, Helmut; Helmchen, Udo; Haag, Friedrich; Schneider, André; Stahl, Rolf A.K.

In: J AM SOC NEPHROL, Vol. 18, No. 7, 7, 2007, p. 2071-2084.

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

Harvard

Panzer, U, Steinmetz, O, Paust, H-J, Meyer-Schwesinger, C, Peters, A, Turner, JE, Zahner, G, Heymann, F, Kurts, C, Hopfer, H, Helmchen, U, Haag, F, Schneider, A & Stahl, RAK 2007, 'Chemokine receptor CXCR3 mediates T cell recruitment and tissue injury in nephrotoxic nephritis in mice.', J AM SOC NEPHROL, vol. 18, no. 7, 7, pp. 2071-2084. <http://www.ncbi.nlm.nih.gov/pubmed/17538187?dopt=Citation>

APA

Panzer, U., Steinmetz, O., Paust, H-J., Meyer-Schwesinger, C., Peters, A., Turner, J. E., Zahner, G., Heymann, F., Kurts, C., Hopfer, H., Helmchen, U., Haag, F., Schneider, A., & Stahl, R. A. K. (2007). Chemokine receptor CXCR3 mediates T cell recruitment and tissue injury in nephrotoxic nephritis in mice. J AM SOC NEPHROL, 18(7), 2071-2084. [7]. http://www.ncbi.nlm.nih.gov/pubmed/17538187?dopt=Citation

Vancouver

Panzer U, Steinmetz O, Paust H-J, Meyer-Schwesinger C, Peters A, Turner JE et al. Chemokine receptor CXCR3 mediates T cell recruitment and tissue injury in nephrotoxic nephritis in mice. J AM SOC NEPHROL. 2007;18(7):2071-2084. 7.

Bibtex

@article{a57a43ed77a24d748990bceb23891419,
title = "Chemokine receptor CXCR3 mediates T cell recruitment and tissue injury in nephrotoxic nephritis in mice.",
abstract = "The chemokine receptor CXCR3 is highly expressed on Th1 polarized T cells and has been predicted to play an important role in T cell recruitment and immune response in a number of inflammatory and autoimmune diseases. For testing whether CXCR3 plays a role in renal inflammation, CXCR3-deficient mice were generated and nephrotoxic nephritis was induced in C57BL/6 CXCR3(-/-) and C57BL/6 wild-type mice. Induction of the nephrotoxic nephritis leads to an increased renal mRNA expression of IP-10/CXCL10 (8.6-fold), Mig/CXCL9 (2.3-fold), and I-TAC/CXCL11 (4.9-fold) during the autologous phase at days 7 and 14. This increased chemokine expression was paralleled by the renal infiltration of T cells, followed by renal tissue injury, albuminuria, and loss of renal function. Compared with wild-type mice, CXCR3-deficient mice had significantly reduced renal T cell infiltrates. Moreover, CXCR3(-/-) mice developed less severe nephritis, with significantly lower albuminuria, better renal function, and a reduced frequency of glomerular crescent formation. Nephritic wild-type and CXCR3(-/-) mice both elicited an efficient systemic nephritogenic immune response in terms of antigen-specific IgG production and IFN-gamma expression by splenocytes in response to the nephritogenic antigen. These findings indicate that the ameliorated nephritis in CXCR3-deficient mice is due to impaired renal trafficking of effector T cells rather than their inability to mount an efficient humoral or cellular immune response. The neutralization of CXCR3 might be a promising therapeutic strategy for Th1-dependent inflammatory renal disease.",
author = "Ulf Panzer and Oliver Steinmetz and Hans-Joachim Paust and Catherine Meyer-Schwesinger and Anett Peters and Turner, {Jan Eric} and Gunther Zahner and Felix Heymann and Christian Kurts and Helmut Hopfer and Udo Helmchen and Friedrich Haag and Andr{\'e} Schneider and Stahl, {Rolf A.K.}",
year = "2007",
language = "Deutsch",
volume = "18",
pages = "2071--2084",
journal = "J AM SOC NEPHROL",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "7",

}

RIS

TY - JOUR

T1 - Chemokine receptor CXCR3 mediates T cell recruitment and tissue injury in nephrotoxic nephritis in mice.

AU - Panzer, Ulf

AU - Steinmetz, Oliver

AU - Paust, Hans-Joachim

AU - Meyer-Schwesinger, Catherine

AU - Peters, Anett

AU - Turner, Jan Eric

AU - Zahner, Gunther

AU - Heymann, Felix

AU - Kurts, Christian

AU - Hopfer, Helmut

AU - Helmchen, Udo

AU - Haag, Friedrich

AU - Schneider, André

AU - Stahl, Rolf A.K.

PY - 2007

Y1 - 2007

N2 - The chemokine receptor CXCR3 is highly expressed on Th1 polarized T cells and has been predicted to play an important role in T cell recruitment and immune response in a number of inflammatory and autoimmune diseases. For testing whether CXCR3 plays a role in renal inflammation, CXCR3-deficient mice were generated and nephrotoxic nephritis was induced in C57BL/6 CXCR3(-/-) and C57BL/6 wild-type mice. Induction of the nephrotoxic nephritis leads to an increased renal mRNA expression of IP-10/CXCL10 (8.6-fold), Mig/CXCL9 (2.3-fold), and I-TAC/CXCL11 (4.9-fold) during the autologous phase at days 7 and 14. This increased chemokine expression was paralleled by the renal infiltration of T cells, followed by renal tissue injury, albuminuria, and loss of renal function. Compared with wild-type mice, CXCR3-deficient mice had significantly reduced renal T cell infiltrates. Moreover, CXCR3(-/-) mice developed less severe nephritis, with significantly lower albuminuria, better renal function, and a reduced frequency of glomerular crescent formation. Nephritic wild-type and CXCR3(-/-) mice both elicited an efficient systemic nephritogenic immune response in terms of antigen-specific IgG production and IFN-gamma expression by splenocytes in response to the nephritogenic antigen. These findings indicate that the ameliorated nephritis in CXCR3-deficient mice is due to impaired renal trafficking of effector T cells rather than their inability to mount an efficient humoral or cellular immune response. The neutralization of CXCR3 might be a promising therapeutic strategy for Th1-dependent inflammatory renal disease.

AB - The chemokine receptor CXCR3 is highly expressed on Th1 polarized T cells and has been predicted to play an important role in T cell recruitment and immune response in a number of inflammatory and autoimmune diseases. For testing whether CXCR3 plays a role in renal inflammation, CXCR3-deficient mice were generated and nephrotoxic nephritis was induced in C57BL/6 CXCR3(-/-) and C57BL/6 wild-type mice. Induction of the nephrotoxic nephritis leads to an increased renal mRNA expression of IP-10/CXCL10 (8.6-fold), Mig/CXCL9 (2.3-fold), and I-TAC/CXCL11 (4.9-fold) during the autologous phase at days 7 and 14. This increased chemokine expression was paralleled by the renal infiltration of T cells, followed by renal tissue injury, albuminuria, and loss of renal function. Compared with wild-type mice, CXCR3-deficient mice had significantly reduced renal T cell infiltrates. Moreover, CXCR3(-/-) mice developed less severe nephritis, with significantly lower albuminuria, better renal function, and a reduced frequency of glomerular crescent formation. Nephritic wild-type and CXCR3(-/-) mice both elicited an efficient systemic nephritogenic immune response in terms of antigen-specific IgG production and IFN-gamma expression by splenocytes in response to the nephritogenic antigen. These findings indicate that the ameliorated nephritis in CXCR3-deficient mice is due to impaired renal trafficking of effector T cells rather than their inability to mount an efficient humoral or cellular immune response. The neutralization of CXCR3 might be a promising therapeutic strategy for Th1-dependent inflammatory renal disease.

M3 - SCORING: Zeitschriftenaufsatz

VL - 18

SP - 2071

EP - 2084

JO - J AM SOC NEPHROL

JF - J AM SOC NEPHROL

SN - 1046-6673

IS - 7

M1 - 7

ER -