Research ExplorerPublicationsCC Chemokine Ligand 18 in ANCA-Associated Crescentic GN

CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN

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CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN. / Brix, Silke R; Stege, Gesa; Disteldorf, Erik; Hoxha, Elion; Krebs, Christian; Krohn, Sonja; Otto, Benjamin; Klätschke, Kristin; Herden, Elisabeth; Heymann, Felix; Lira, Sergio A; Tacke, Frank; Wolf, Gunter; Busch, Martin; Jabs, Wolfram J; Özcan, Fedai; Keller, Frieder; Beige, Joachim; Wagner, Karl; Helmchen, Udo; Noriega, Maria de las Mercedes; Wiech, Thorsten; Panzer, Ulf; Stahl, Rolf A K.

In: J AM SOC NEPHROL, Vol. 26, No. 9, 11.03.2015, p. 2105-2117.

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

Harvard

Brix, SR, Stege, G, Disteldorf, E, Hoxha, E, Krebs, C, Krohn, S, Otto, B, Klätschke, K, Herden, E, Heymann, F, Lira, SA, Tacke, F, Wolf, G, Busch, M, Jabs, WJ, Özcan, F, Keller, F, Beige, J, Wagner, K, Helmchen, U, Noriega, MDLM, Wiech, T, Panzer, U & Stahl, RAK 2015, 'CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN', J AM SOC NEPHROL, vol. 26, no. 9, pp. 2105-2117. https://doi.org/10.1681/ASN.2014040407

APA

Brix, S. R., Stege, G., Disteldorf, E., Hoxha, E., Krebs, C., Krohn, S., Otto, B., Klätschke, K., Herden, E., Heymann, F., Lira, S. A., Tacke, F., Wolf, G., Busch, M., Jabs, W. J., Özcan, F., Keller, F., Beige, J., Wagner, K., ... Stahl, R. A. K. (2015). CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN. J AM SOC NEPHROL, 26(9), 2105-2117. https://doi.org/10.1681/ASN.2014040407

Vancouver

Brix SR, Stege G, Disteldorf E, Hoxha E, Krebs C, Krohn S et al. CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN. J AM SOC NEPHROL. 2015 Mar 11;26(9):2105-2117. https://doi.org/10.1681/ASN.2014040407

Bibtex

@article{6907a043b988444090af31b2b9075c86,
title = "CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN",
abstract = "ANCA-associated vasculitis is the most frequent cause of crescentic GN. To define new molecular and/or cellular biomarkers of this disease in the kidney, we performed microarray analyses of renal biopsy samples from patients with ANCA-associated crescentic GN. Expression profiles were correlated with clinical data in a prospective study of patients with renal ANCA disease. CC chemokine ligand 18 (CCL18), acting through CC chemokine receptor 8 (CCR8) on mononuclear cells, was identified as the most upregulated chemotactic cytokine in patients with newly diagnosed ANCA-associated crescentic GN. Macrophages and myeloid dendritic cells in the kidney were detected as CCL18-producing cells. The density of CCL18(+) cells correlated with crescent formation, interstitial inflammation, and impairment of renal function. CCL18 protein levels were higher in sera of patients with renal ANCA disease compared with those in sera of patients with other forms of crescentic GN. CCL18 serum levels were higher in patients who suffered from ANCA-associated renal relapses compared with those in patients who remained in remission. Using a murine model of crescentic GN, we explored the effects of the CCL18 murine functional analog CCL8 and its receptor CCR8 on kidney function and morphology. Compared with wild-type mice, Ccr8(-/-) mice had significantly less infiltration of pathogenic mononuclear phagocytes. Furthermore, Ccr8(-/-) mice maintained renal function better and had reduced renal tissue injury. In summary, our data indicate that CCL18 drives renal inflammation through CCR8-expressing cells and could serve as a biomarker for disease activity and renal relapse in ANCA-associated crescentic GN.",
author = "Brix, {Silke R} and Gesa Stege and Erik Disteldorf and Elion Hoxha and Christian Krebs and Sonja Krohn and Benjamin Otto and Kristin Kl{\"a}tschke and Elisabeth Herden and Felix Heymann and Lira, {Sergio A} and Frank Tacke and Gunter Wolf and Martin Busch and Jabs, {Wolfram J} and Fedai {\"O}zcan and Frieder Keller and Joachim Beige and Karl Wagner and Udo Helmchen and Noriega, {Maria de las Mercedes} and Thorsten Wiech and Ulf Panzer and Stahl, {Rolf A K}",
note = "Copyright {\textcopyright} 2015 by the American Society of Nephrology.",
year = "2015",
month = mar,
day = "11",
doi = "10.1681/ASN.2014040407",
language = "English",
volume = "26",
pages = "2105--2117",
journal = "J AM SOC NEPHROL",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "9",

}

RIS

TY - JOUR

T1 - CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN

AU - Brix, Silke R

AU - Stege, Gesa

AU - Disteldorf, Erik

AU - Hoxha, Elion

AU - Krebs, Christian

AU - Krohn, Sonja

AU - Otto, Benjamin

AU - Klätschke, Kristin

AU - Herden, Elisabeth

AU - Heymann, Felix

AU - Lira, Sergio A

AU - Tacke, Frank

AU - Wolf, Gunter

AU - Busch, Martin

AU - Jabs, Wolfram J

AU - Özcan, Fedai

AU - Keller, Frieder

AU - Beige, Joachim

AU - Wagner, Karl

AU - Helmchen, Udo

AU - Noriega, Maria de las Mercedes

AU - Wiech, Thorsten

AU - Panzer, Ulf

AU - Stahl, Rolf A K

N1 - Copyright © 2015 by the American Society of Nephrology.

PY - 2015/3/11

Y1 - 2015/3/11

N2 - ANCA-associated vasculitis is the most frequent cause of crescentic GN. To define new molecular and/or cellular biomarkers of this disease in the kidney, we performed microarray analyses of renal biopsy samples from patients with ANCA-associated crescentic GN. Expression profiles were correlated with clinical data in a prospective study of patients with renal ANCA disease. CC chemokine ligand 18 (CCL18), acting through CC chemokine receptor 8 (CCR8) on mononuclear cells, was identified as the most upregulated chemotactic cytokine in patients with newly diagnosed ANCA-associated crescentic GN. Macrophages and myeloid dendritic cells in the kidney were detected as CCL18-producing cells. The density of CCL18(+) cells correlated with crescent formation, interstitial inflammation, and impairment of renal function. CCL18 protein levels were higher in sera of patients with renal ANCA disease compared with those in sera of patients with other forms of crescentic GN. CCL18 serum levels were higher in patients who suffered from ANCA-associated renal relapses compared with those in patients who remained in remission. Using a murine model of crescentic GN, we explored the effects of the CCL18 murine functional analog CCL8 and its receptor CCR8 on kidney function and morphology. Compared with wild-type mice, Ccr8(-/-) mice had significantly less infiltration of pathogenic mononuclear phagocytes. Furthermore, Ccr8(-/-) mice maintained renal function better and had reduced renal tissue injury. In summary, our data indicate that CCL18 drives renal inflammation through CCR8-expressing cells and could serve as a biomarker for disease activity and renal relapse in ANCA-associated crescentic GN.

AB - ANCA-associated vasculitis is the most frequent cause of crescentic GN. To define new molecular and/or cellular biomarkers of this disease in the kidney, we performed microarray analyses of renal biopsy samples from patients with ANCA-associated crescentic GN. Expression profiles were correlated with clinical data in a prospective study of patients with renal ANCA disease. CC chemokine ligand 18 (CCL18), acting through CC chemokine receptor 8 (CCR8) on mononuclear cells, was identified as the most upregulated chemotactic cytokine in patients with newly diagnosed ANCA-associated crescentic GN. Macrophages and myeloid dendritic cells in the kidney were detected as CCL18-producing cells. The density of CCL18(+) cells correlated with crescent formation, interstitial inflammation, and impairment of renal function. CCL18 protein levels were higher in sera of patients with renal ANCA disease compared with those in sera of patients with other forms of crescentic GN. CCL18 serum levels were higher in patients who suffered from ANCA-associated renal relapses compared with those in patients who remained in remission. Using a murine model of crescentic GN, we explored the effects of the CCL18 murine functional analog CCL8 and its receptor CCR8 on kidney function and morphology. Compared with wild-type mice, Ccr8(-/-) mice had significantly less infiltration of pathogenic mononuclear phagocytes. Furthermore, Ccr8(-/-) mice maintained renal function better and had reduced renal tissue injury. In summary, our data indicate that CCL18 drives renal inflammation through CCR8-expressing cells and could serve as a biomarker for disease activity and renal relapse in ANCA-associated crescentic GN.

U2 - 10.1681/ASN.2014040407

DO - 10.1681/ASN.2014040407

M3 - SCORING: Journal article

C2 - 25762060

VL - 26

SP - 2105

EP - 2117

JO - J AM SOC NEPHROL

JF - J AM SOC NEPHROL

SN - 1046-6673

IS - 9

ER -