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Exclusive CX3CR1 dependence of kidney DCs impacts glomerulonephritis progression

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Exclusive CX3CR1 dependence of kidney DCs impacts glomerulonephritis progression. / Hochheiser, Katharina; Heuser, Christoph; Krause, Torsten A; Teteris, Simon; Ilias, Anissa; Weisheit, Christina; Hoss, Florian; Tittel, André P; Knolle, Percy A; Panzer, Ulf; Engel, Daniel R; Tharaux, Pierre-Louis; Kurts, Christian.

In: J CLIN INVEST, Vol. 123, No. 10, 01.10.2013, p. 4242-54.

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

Harvard

Hochheiser, K, Heuser, C, Krause, TA, Teteris, S, Ilias, A, Weisheit, C, Hoss, F, Tittel, AP, Knolle, PA, Panzer, U, Engel, DR, Tharaux, P-L & Kurts, C 2013, 'Exclusive CX3CR1 dependence of kidney DCs impacts glomerulonephritis progression', J CLIN INVEST, vol. 123, no. 10, pp. 4242-54. https://doi.org/10.1172/JCI70143

APA

Hochheiser, K., Heuser, C., Krause, T. A., Teteris, S., Ilias, A., Weisheit, C., Hoss, F., Tittel, A. P., Knolle, P. A., Panzer, U., Engel, D. R., Tharaux, P-L., & Kurts, C. (2013). Exclusive CX3CR1 dependence of kidney DCs impacts glomerulonephritis progression. J CLIN INVEST, 123(10), 4242-54. https://doi.org/10.1172/JCI70143

Vancouver

Hochheiser K, Heuser C, Krause TA, Teteris S, Ilias A, Weisheit C et al. Exclusive CX3CR1 dependence of kidney DCs impacts glomerulonephritis progression. J CLIN INVEST. 2013 Oct 1;123(10):4242-54. https://doi.org/10.1172/JCI70143

Bibtex

@article{0e733dc493974a81987adc4e676591d1,
title = "Exclusive CX3CR1 dependence of kidney DCs impacts glomerulonephritis progression",
abstract = "DCs and macrophages both express the chemokine receptor CX3CR1. Here we demonstrate that its ligand, CX3CL1, is highly expressed in the murine kidney and intestine. CX3CR1 deficiency markedly reduced DC numbers in the healthy and inflamed kidney cortex, and to a lesser degree in the kidney medulla and intestine, but not in other organs. CX3CR1 also promoted influx of DC precursors in crescentic glomerulonephritis, a DC-dependent aggressive type of nephritis. Disease severity was strongly attenuated in CX3CR1-deficient mice. Primarily CX3CR1-dependent DCs in the kidney cortex processed antigen for the intrarenal stimulation of T helper cells, a function important for glomerulonephritis progression. In contrast, medullary DCs played a specialized role in inducing innate immunity against bacterial pyelonephritis by recruiting neutrophils through rapid chemokine production. CX3CR1 deficiency had little effect on the immune defense against pyelonephritis, as medullary DCs were less CX3CR1 dependent than cortical DCs and because recruited neutrophils produced chemokines to compensate for the DC paucity. These findings demonstrate that cortical and medullary DCs play specialized roles in their respective kidney compartments. We identify CX3CR1 as a potential therapeutic target in glomerulonephritis that may involve fewer adverse side effects, such as impaired anti-infectious defense or compromised DC functions in other organs.",
keywords = "Animals, Antigen Presentation, Cells, Cultured, Dendritic Cells, Disease Progression, Female, Glomerulonephritis, Histocompatibility Antigens Class II, Immunity, Innate, Kidney, Macrophages, Mice, Mice, Inbred C57BL, Mice, Transgenic, Pyelonephritis, Receptors, Chemokine, T-Lymphocytes, Helper-Inducer",
author = "Katharina Hochheiser and Christoph Heuser and Krause, {Torsten A} and Simon Teteris and Anissa Ilias and Christina Weisheit and Florian Hoss and Tittel, {Andr{\'e} P} and Knolle, {Percy A} and Ulf Panzer and Engel, {Daniel R} and Pierre-Louis Tharaux and Christian Kurts",
year = "2013",
month = oct,
day = "1",
doi = "10.1172/JCI70143",
language = "English",
volume = "123",
pages = "4242--54",
journal = "J CLIN INVEST",
issn = "0021-9738",
publisher = "The American Society for Clinical Investigation",
number = "10",

}

RIS

TY - JOUR

T1 - Exclusive CX3CR1 dependence of kidney DCs impacts glomerulonephritis progression

AU - Hochheiser, Katharina

AU - Heuser, Christoph

AU - Krause, Torsten A

AU - Teteris, Simon

AU - Ilias, Anissa

AU - Weisheit, Christina

AU - Hoss, Florian

AU - Tittel, André P

AU - Knolle, Percy A

AU - Panzer, Ulf

AU - Engel, Daniel R

AU - Tharaux, Pierre-Louis

AU - Kurts, Christian

PY - 2013/10/1

Y1 - 2013/10/1

N2 - DCs and macrophages both express the chemokine receptor CX3CR1. Here we demonstrate that its ligand, CX3CL1, is highly expressed in the murine kidney and intestine. CX3CR1 deficiency markedly reduced DC numbers in the healthy and inflamed kidney cortex, and to a lesser degree in the kidney medulla and intestine, but not in other organs. CX3CR1 also promoted influx of DC precursors in crescentic glomerulonephritis, a DC-dependent aggressive type of nephritis. Disease severity was strongly attenuated in CX3CR1-deficient mice. Primarily CX3CR1-dependent DCs in the kidney cortex processed antigen for the intrarenal stimulation of T helper cells, a function important for glomerulonephritis progression. In contrast, medullary DCs played a specialized role in inducing innate immunity against bacterial pyelonephritis by recruiting neutrophils through rapid chemokine production. CX3CR1 deficiency had little effect on the immune defense against pyelonephritis, as medullary DCs were less CX3CR1 dependent than cortical DCs and because recruited neutrophils produced chemokines to compensate for the DC paucity. These findings demonstrate that cortical and medullary DCs play specialized roles in their respective kidney compartments. We identify CX3CR1 as a potential therapeutic target in glomerulonephritis that may involve fewer adverse side effects, such as impaired anti-infectious defense or compromised DC functions in other organs.

AB - DCs and macrophages both express the chemokine receptor CX3CR1. Here we demonstrate that its ligand, CX3CL1, is highly expressed in the murine kidney and intestine. CX3CR1 deficiency markedly reduced DC numbers in the healthy and inflamed kidney cortex, and to a lesser degree in the kidney medulla and intestine, but not in other organs. CX3CR1 also promoted influx of DC precursors in crescentic glomerulonephritis, a DC-dependent aggressive type of nephritis. Disease severity was strongly attenuated in CX3CR1-deficient mice. Primarily CX3CR1-dependent DCs in the kidney cortex processed antigen for the intrarenal stimulation of T helper cells, a function important for glomerulonephritis progression. In contrast, medullary DCs played a specialized role in inducing innate immunity against bacterial pyelonephritis by recruiting neutrophils through rapid chemokine production. CX3CR1 deficiency had little effect on the immune defense against pyelonephritis, as medullary DCs were less CX3CR1 dependent than cortical DCs and because recruited neutrophils produced chemokines to compensate for the DC paucity. These findings demonstrate that cortical and medullary DCs play specialized roles in their respective kidney compartments. We identify CX3CR1 as a potential therapeutic target in glomerulonephritis that may involve fewer adverse side effects, such as impaired anti-infectious defense or compromised DC functions in other organs.

KW - Animals

KW - Antigen Presentation

KW - Cells, Cultured

KW - Dendritic Cells

KW - Disease Progression

KW - Female

KW - Glomerulonephritis

KW - Histocompatibility Antigens Class II

KW - Immunity, Innate

KW - Kidney

KW - Macrophages

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Transgenic

KW - Pyelonephritis

KW - Receptors, Chemokine

KW - T-Lymphocytes, Helper-Inducer

U2 - 10.1172/JCI70143

DO - 10.1172/JCI70143

M3 - SCORING: Journal article

C2 - 23999431

VL - 123

SP - 4242

EP - 4254

JO - J CLIN INVEST

JF - J CLIN INVEST

SN - 0021-9738

IS - 10

ER -