Efficient renal recruitment of macrophages and T cells in mice lacking the duffy antigen/receptor for chemokines

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Efficient renal recruitment of macrophages and T cells in mice lacking the duffy antigen/receptor for chemokines. / Vielhauer, Volker; Allam, Ramanjaneyulu; Lindenmeyer, Maja T; Cohen, Clemens D; Draganovici, Dan; Mandelbaum, Jana; Eltrich, Nuru; Nelson, Peter J; Anders, Hans-Joachim; Pruenster, Monika; Rot, Antal; Schlöndorff, Detlef; Segerer, Stephan.

in: AM J PATHOL, Jahrgang 175, Nr. 1, 07.2009, S. 119-31.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Vielhauer, V, Allam, R, Lindenmeyer, MT, Cohen, CD, Draganovici, D, Mandelbaum, J, Eltrich, N, Nelson, PJ, Anders, H-J, Pruenster, M, Rot, A, Schlöndorff, D & Segerer, S 2009, 'Efficient renal recruitment of macrophages and T cells in mice lacking the duffy antigen/receptor for chemokines', AM J PATHOL, Jg. 175, Nr. 1, S. 119-31. https://doi.org/10.2353/ajpath.2009.080590

APA

Vielhauer, V., Allam, R., Lindenmeyer, M. T., Cohen, C. D., Draganovici, D., Mandelbaum, J., Eltrich, N., Nelson, P. J., Anders, H-J., Pruenster, M., Rot, A., Schlöndorff, D., & Segerer, S. (2009). Efficient renal recruitment of macrophages and T cells in mice lacking the duffy antigen/receptor for chemokines. AM J PATHOL, 175(1), 119-31. https://doi.org/10.2353/ajpath.2009.080590

Vancouver

Bibtex

@article{e6eedb3484874faa8a5044fcfa95d444,
title = "Efficient renal recruitment of macrophages and T cells in mice lacking the duffy antigen/receptor for chemokines",
abstract = "The Duffy antigen/receptor for chemokines (DARC) is a chemokine-binding protein that is expressed on erythrocytes and renal endothelial cells. DARC-mediated endothelial transcytosis of chemokines may facilitate the renal recruitment of macrophages and T cells, as has been suggested for neutrophils. We studied the role of Darc in two mouse models of prolonged renal inflammation, one that primarily involves the tubulointerstitium (unilateral ureteral obstruction), and one that requires an adaptive immune response that leads to glomerulonephritis (accelerated nephrotoxic nephritis). Renal expression of Darc and its ligands was increased in both models. Leukocytes effectively infiltrated obstructed kidneys in Darc-deficient mice with pronounced T-cell infiltration at early time points. Development of interstitial fibrosis was comparable in both genotypes. Nephrotoxic nephritis was inducible in Darc-deficient mice, with both an increased humoral immune response and functional impairment during the early phase of disease. Leukocytes efficiently infiltrated kidneys of Darc-deficient mice, with increased cell numbers at early but not late time points. Taken together, renal inflammation developed more rapidly in DARC-deficient mice, without affecting the extent of renal injury at later time points. Thus, genetic elimination of Darc in mice does not prevent the development of renal infiltrates and may even enhance such development during the early phases of interstitial and glomerular diseases in mouse models of prolonged renal inflammation.",
keywords = "Animals, Chemokines, Chemotaxis, Leukocyte, Duffy Blood-Group System, Enzyme-Linked Immunosorbent Assay, Fibrosis, Flow Cytometry, Glomerulonephritis, Image Processing, Computer-Assisted, Immunoglobulin G, Immunohistochemistry, Macrophages, Mice, Mice, Inbred C57BL, Mice, Knockout, Receptors, Cell Surface, Reverse Transcriptase Polymerase Chain Reaction, T-Lymphocytes, Journal Article, Research Support, Non-U.S. Gov't",
author = "Volker Vielhauer and Ramanjaneyulu Allam and Lindenmeyer, {Maja T} and Cohen, {Clemens D} and Dan Draganovici and Jana Mandelbaum and Nuru Eltrich and Nelson, {Peter J} and Hans-Joachim Anders and Monika Pruenster and Antal Rot and Detlef Schl{\"o}ndorff and Stephan Segerer",
year = "2009",
month = jul,
doi = "10.2353/ajpath.2009.080590",
language = "English",
volume = "175",
pages = "119--31",
journal = "AM J PATHOL",
issn = "0002-9440",
publisher = "Elsevier Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Efficient renal recruitment of macrophages and T cells in mice lacking the duffy antigen/receptor for chemokines

AU - Vielhauer, Volker

AU - Allam, Ramanjaneyulu

AU - Lindenmeyer, Maja T

AU - Cohen, Clemens D

AU - Draganovici, Dan

AU - Mandelbaum, Jana

AU - Eltrich, Nuru

AU - Nelson, Peter J

AU - Anders, Hans-Joachim

AU - Pruenster, Monika

AU - Rot, Antal

AU - Schlöndorff, Detlef

AU - Segerer, Stephan

PY - 2009/7

Y1 - 2009/7

N2 - The Duffy antigen/receptor for chemokines (DARC) is a chemokine-binding protein that is expressed on erythrocytes and renal endothelial cells. DARC-mediated endothelial transcytosis of chemokines may facilitate the renal recruitment of macrophages and T cells, as has been suggested for neutrophils. We studied the role of Darc in two mouse models of prolonged renal inflammation, one that primarily involves the tubulointerstitium (unilateral ureteral obstruction), and one that requires an adaptive immune response that leads to glomerulonephritis (accelerated nephrotoxic nephritis). Renal expression of Darc and its ligands was increased in both models. Leukocytes effectively infiltrated obstructed kidneys in Darc-deficient mice with pronounced T-cell infiltration at early time points. Development of interstitial fibrosis was comparable in both genotypes. Nephrotoxic nephritis was inducible in Darc-deficient mice, with both an increased humoral immune response and functional impairment during the early phase of disease. Leukocytes efficiently infiltrated kidneys of Darc-deficient mice, with increased cell numbers at early but not late time points. Taken together, renal inflammation developed more rapidly in DARC-deficient mice, without affecting the extent of renal injury at later time points. Thus, genetic elimination of Darc in mice does not prevent the development of renal infiltrates and may even enhance such development during the early phases of interstitial and glomerular diseases in mouse models of prolonged renal inflammation.

AB - The Duffy antigen/receptor for chemokines (DARC) is a chemokine-binding protein that is expressed on erythrocytes and renal endothelial cells. DARC-mediated endothelial transcytosis of chemokines may facilitate the renal recruitment of macrophages and T cells, as has been suggested for neutrophils. We studied the role of Darc in two mouse models of prolonged renal inflammation, one that primarily involves the tubulointerstitium (unilateral ureteral obstruction), and one that requires an adaptive immune response that leads to glomerulonephritis (accelerated nephrotoxic nephritis). Renal expression of Darc and its ligands was increased in both models. Leukocytes effectively infiltrated obstructed kidneys in Darc-deficient mice with pronounced T-cell infiltration at early time points. Development of interstitial fibrosis was comparable in both genotypes. Nephrotoxic nephritis was inducible in Darc-deficient mice, with both an increased humoral immune response and functional impairment during the early phase of disease. Leukocytes efficiently infiltrated kidneys of Darc-deficient mice, with increased cell numbers at early but not late time points. Taken together, renal inflammation developed more rapidly in DARC-deficient mice, without affecting the extent of renal injury at later time points. Thus, genetic elimination of Darc in mice does not prevent the development of renal infiltrates and may even enhance such development during the early phases of interstitial and glomerular diseases in mouse models of prolonged renal inflammation.

KW - Animals

KW - Chemokines

KW - Chemotaxis, Leukocyte

KW - Duffy Blood-Group System

KW - Enzyme-Linked Immunosorbent Assay

KW - Fibrosis

KW - Flow Cytometry

KW - Glomerulonephritis

KW - Image Processing, Computer-Assisted

KW - Immunoglobulin G

KW - Immunohistochemistry

KW - Macrophages

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Receptors, Cell Surface

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - T-Lymphocytes

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.2353/ajpath.2009.080590

DO - 10.2353/ajpath.2009.080590

M3 - SCORING: Journal article

C2 - 19498001

VL - 175

SP - 119

EP - 131

JO - AM J PATHOL

JF - AM J PATHOL

SN - 0002-9440

IS - 1

ER -