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CD103+ Kidney Dendritic Cells Protect against Crescentic GN by Maintaining IL-10-Producing Regulatory T Cells

Standard

CD103+ Kidney Dendritic Cells Protect against Crescentic GN by Maintaining IL-10-Producing Regulatory T Cells. / Evers, Beatrix D G; Engel, Daniel R; Böhner, Alexander M C; Tittel, André P; Krause, Torsten A; Heuser, Christoph; Garbi, Natalio; Kastenmüller, Wolfgang; Mack, Matthias; Tiegs, Gisa; Panzer, Ulf; Boor, Peter; Ludwig-Portugall, Isis; Kurts, Christian.

in: J AM SOC NEPHROL, Jahrgang 27, Nr. 11, 11.2016, S. 3368-3382.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Evers, BDG, Engel, DR, Böhner, AMC, Tittel, AP, Krause, TA, Heuser, C, Garbi, N, Kastenmüller, W, Mack, M, Tiegs, G, Panzer, U, Boor, P, Ludwig-Portugall, I & Kurts, C 2016, 'CD103+ Kidney Dendritic Cells Protect against Crescentic GN by Maintaining IL-10-Producing Regulatory T Cells', J AM SOC NEPHROL, Jg. 27, Nr. 11, S. 3368-3382. https://doi.org/10.1681/ASN.2015080873

APA

Evers, B. D. G., Engel, D. R., Böhner, A. M. C., Tittel, A. P., Krause, T. A., Heuser, C., Garbi, N., Kastenmüller, W., Mack, M., Tiegs, G., Panzer, U., Boor, P., Ludwig-Portugall, I., & Kurts, C. (2016). CD103+ Kidney Dendritic Cells Protect against Crescentic GN by Maintaining IL-10-Producing Regulatory T Cells. J AM SOC NEPHROL, 27(11), 3368-3382. https://doi.org/10.1681/ASN.2015080873

Vancouver

Evers BDG, Engel DR, Böhner AMC, Tittel AP, Krause TA, Heuser C et al. CD103+ Kidney Dendritic Cells Protect against Crescentic GN by Maintaining IL-10-Producing Regulatory T Cells. J AM SOC NEPHROL. 2016 Nov;27(11):3368-3382. https://doi.org/10.1681/ASN.2015080873

Bibtex

@article{f95f07a6232844e4bae56e475d2b84de,
title = "CD103+ Kidney Dendritic Cells Protect against Crescentic GN by Maintaining IL-10-Producing Regulatory T Cells",
abstract = "Kidney dendritic cells (DCs) regulate nephritogenic T cell responses. Most kidney DCs belong to the CD11b(+) subset and promote crescentic GN (cGN). The function of the CD103(+) subset, which represents <5% of kidney DCs, is poorly understood. We studied the role of CD103(+) DCs in cGN using several lines of genetically modified mice that allowed us to reduce the number of these cells. In all lines, we detected a reduction of FoxP3(+) intrarenal regulatory T cells (Tregs), which protect against cGN. Mice lacking the transcription factor Batf3 had a more profound reduction of CD103(+) DCs and Tregs than did the other lines used, and showed the most profound aggravation of cGN. The conditional reduction of CD103(+) DC numbers by 50% in Langerin-DTR mice halved Treg numbers, which did not suffice to significantly aggravate cGN. Mice lacking the cytokine Flt3L had fewer CD103(+) DCs and Tregs than Langerin-DTR mice but exhibited milder cGN than did Batf3(-/-) mice presumably because proinflammatory CD11b(+) DCs were somewhat depleted as well. Conversely, Flt3L supplementation increased the number of CD103(+) DCs and Tregs, but also of proinflammatory CD11b(+) DCs. On antibody-mediated removal of CD11b(+) DCs, Flt3L supplementation ameliorated cGN. Mechanistically, CD103(+) DCs caused cocultured T cells to differentiate into Tregs and produced the chemokine CCL20, which is known to attract Tregs into the kidney. Our findings show that CD103(+) DCs foster intrarenal FoxP3(+) Treg accumulation, thereby antagonizing proinflammatory CD11b(+) DCs. Thus, increasing CD103(+) DC numbers or functionality might be advantageous in cGN.",
keywords = "Animals, Antigens, CD, Dendritic Cells, Glomerulonephritis, Integrin alpha Chains, Interleukin-10, Kidney, Mice, Mice, Inbred C57BL, T-Lymphocytes, Regulatory, Journal Article",
author = "Evers, {Beatrix D G} and Engel, {Daniel R} and B{\"o}hner, {Alexander M C} and Tittel, {Andr{\'e} P} and Krause, {Torsten A} and Christoph Heuser and Natalio Garbi and Wolfgang Kastenm{\"u}ller and Matthias Mack and Gisa Tiegs and Ulf Panzer and Peter Boor and Isis Ludwig-Portugall and Christian Kurts",
note = "Copyright {\textcopyright} 2016 by the American Society of Nephrology.",
year = "2016",
month = nov,
doi = "10.1681/ASN.2015080873",
language = "English",
volume = "27",
pages = "3368--3382",
journal = "J AM SOC NEPHROL",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "11",

}

RIS

TY - JOUR

T1 - CD103+ Kidney Dendritic Cells Protect against Crescentic GN by Maintaining IL-10-Producing Regulatory T Cells

AU - Evers, Beatrix D G

AU - Engel, Daniel R

AU - Böhner, Alexander M C

AU - Tittel, André P

AU - Krause, Torsten A

AU - Heuser, Christoph

AU - Garbi, Natalio

AU - Kastenmüller, Wolfgang

AU - Mack, Matthias

AU - Tiegs, Gisa

AU - Panzer, Ulf

AU - Boor, Peter

AU - Ludwig-Portugall, Isis

AU - Kurts, Christian

N1 - Copyright © 2016 by the American Society of Nephrology.

PY - 2016/11

Y1 - 2016/11

N2 - Kidney dendritic cells (DCs) regulate nephritogenic T cell responses. Most kidney DCs belong to the CD11b(+) subset and promote crescentic GN (cGN). The function of the CD103(+) subset, which represents <5% of kidney DCs, is poorly understood. We studied the role of CD103(+) DCs in cGN using several lines of genetically modified mice that allowed us to reduce the number of these cells. In all lines, we detected a reduction of FoxP3(+) intrarenal regulatory T cells (Tregs), which protect against cGN. Mice lacking the transcription factor Batf3 had a more profound reduction of CD103(+) DCs and Tregs than did the other lines used, and showed the most profound aggravation of cGN. The conditional reduction of CD103(+) DC numbers by 50% in Langerin-DTR mice halved Treg numbers, which did not suffice to significantly aggravate cGN. Mice lacking the cytokine Flt3L had fewer CD103(+) DCs and Tregs than Langerin-DTR mice but exhibited milder cGN than did Batf3(-/-) mice presumably because proinflammatory CD11b(+) DCs were somewhat depleted as well. Conversely, Flt3L supplementation increased the number of CD103(+) DCs and Tregs, but also of proinflammatory CD11b(+) DCs. On antibody-mediated removal of CD11b(+) DCs, Flt3L supplementation ameliorated cGN. Mechanistically, CD103(+) DCs caused cocultured T cells to differentiate into Tregs and produced the chemokine CCL20, which is known to attract Tregs into the kidney. Our findings show that CD103(+) DCs foster intrarenal FoxP3(+) Treg accumulation, thereby antagonizing proinflammatory CD11b(+) DCs. Thus, increasing CD103(+) DC numbers or functionality might be advantageous in cGN.

AB - Kidney dendritic cells (DCs) regulate nephritogenic T cell responses. Most kidney DCs belong to the CD11b(+) subset and promote crescentic GN (cGN). The function of the CD103(+) subset, which represents <5% of kidney DCs, is poorly understood. We studied the role of CD103(+) DCs in cGN using several lines of genetically modified mice that allowed us to reduce the number of these cells. In all lines, we detected a reduction of FoxP3(+) intrarenal regulatory T cells (Tregs), which protect against cGN. Mice lacking the transcription factor Batf3 had a more profound reduction of CD103(+) DCs and Tregs than did the other lines used, and showed the most profound aggravation of cGN. The conditional reduction of CD103(+) DC numbers by 50% in Langerin-DTR mice halved Treg numbers, which did not suffice to significantly aggravate cGN. Mice lacking the cytokine Flt3L had fewer CD103(+) DCs and Tregs than Langerin-DTR mice but exhibited milder cGN than did Batf3(-/-) mice presumably because proinflammatory CD11b(+) DCs were somewhat depleted as well. Conversely, Flt3L supplementation increased the number of CD103(+) DCs and Tregs, but also of proinflammatory CD11b(+) DCs. On antibody-mediated removal of CD11b(+) DCs, Flt3L supplementation ameliorated cGN. Mechanistically, CD103(+) DCs caused cocultured T cells to differentiate into Tregs and produced the chemokine CCL20, which is known to attract Tregs into the kidney. Our findings show that CD103(+) DCs foster intrarenal FoxP3(+) Treg accumulation, thereby antagonizing proinflammatory CD11b(+) DCs. Thus, increasing CD103(+) DC numbers or functionality might be advantageous in cGN.

KW - Animals

KW - Antigens, CD

KW - Dendritic Cells

KW - Glomerulonephritis

KW - Integrin alpha Chains

KW - Interleukin-10

KW - Kidney

KW - Mice

KW - Mice, Inbred C57BL

KW - T-Lymphocytes, Regulatory

KW - Journal Article

U2 - 10.1681/ASN.2015080873

DO - 10.1681/ASN.2015080873

M3 - SCORING: Journal article

C2 - 27036736

VL - 27

SP - 3368

EP - 3382

JO - J AM SOC NEPHROL

JF - J AM SOC NEPHROL

SN - 1046-6673

IS - 11

ER -