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MicroRNA-155 drives TH17 immune response and tissue injury in experimental crescentic GN

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MicroRNA-155 drives TH17 immune response and tissue injury in experimental crescentic GN. / Krebs, Christian F; Kapffer, Sonja; Paust, Hans-Joachim; Schmidt, Tilman; Bennstein, Sabrina B; Peters, Anett; Stege, Gesa; Brix, Silke R; Meyer-Schwesinger, Catherine; Müller, Roman-Ulrich; Turner, Jan Eric; Steinmetz, Oliver M; Wolf, Gunter; Stahl, Rolf A K; Panzer, Ulf.

in: J AM SOC NEPHROL, Jahrgang 24, Nr. 12, 01.12.2013, S. 1955-65.

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

Harvard

Krebs, CF, Kapffer, S, Paust, H-J, Schmidt, T, Bennstein, SB, Peters, A, Stege, G, Brix, SR, Meyer-Schwesinger, C, Müller, R-U, Turner, JE, Steinmetz, OM, Wolf, G, Stahl, RAK & Panzer, U 2013, 'MicroRNA-155 drives TH17 immune response and tissue injury in experimental crescentic GN', J AM SOC NEPHROL, Jg. 24, Nr. 12, S. 1955-65. https://doi.org/10.1681/ASN.2013020130

APA

Krebs, C. F., Kapffer, S., Paust, H-J., Schmidt, T., Bennstein, S. B., Peters, A., Stege, G., Brix, S. R., Meyer-Schwesinger, C., Müller, R-U., Turner, J. E., Steinmetz, O. M., Wolf, G., Stahl, R. A. K., & Panzer, U. (2013). MicroRNA-155 drives TH17 immune response and tissue injury in experimental crescentic GN. J AM SOC NEPHROL, 24(12), 1955-65. https://doi.org/10.1681/ASN.2013020130

Vancouver

Krebs CF, Kapffer S, Paust H-J, Schmidt T, Bennstein SB, Peters A et al. MicroRNA-155 drives TH17 immune response and tissue injury in experimental crescentic GN. J AM SOC NEPHROL. 2013 Dez 1;24(12):1955-65. https://doi.org/10.1681/ASN.2013020130

Bibtex

@article{c4c407aa945d4319a01dbdb44a593980,
title = "MicroRNA-155 drives TH17 immune response and tissue injury in experimental crescentic GN",
abstract = "CD4(+) T cells play a pivotal role in the pathogenesis of autoimmune disease, including human and experimental crescentic GN. Micro-RNAs (miRs) have emerged as important regulators of immune cell development, but the impact of miRs on the regulation of the CD4(+) T cell immune response remains to be fully clarified. Here, we report that miR-155 expression is upregulated in the kidneys of patients with ANCA-associated crescentic GN and a murine model of crescentic GN (nephrotoxic nephritis). To elucidate the potential role of miR-155 in T cell-mediated inflammation, nephritis was induced in miR-155(-/-) and wild-type mice. The systemic and renal nephritogenic TH17 immune response decreased markedly in nephritic miR-155(-/-) mice. Consistent with this finding, miR-155-deficient mice developed less severe nephritis, with reduced histologic and functional injury. Adoptive transfer of miR-155(-/-) and wild-type CD4(+) T cells into nephritic recombination activating gene 1-deficient (Rag-1(-/-)) mice showed the T cell-intrinsic importance of miR-155 for the stability of pathogenic TH17 immunity. These findings indicate that miR-155 drives the TH17 immune response and tissue injury in experimental crescentic GN and show that miR-155 is a potential therapeutic target in TH17-mediated diseases.",
keywords = "Animals, Cells, Cultured, Disease Models, Animal, Glomerulonephritis, Humans, Immunity, Humoral, Immunophenotyping, Male, Mice, Mice, Congenic, Mice, Inbred C57BL, Mice, Mutant Strains, MicroRNAs, Neutrophils, Spleen, Th17 Cells",
author = "Krebs, {Christian F} and Sonja Kapffer and Hans-Joachim Paust and Tilman Schmidt and Bennstein, {Sabrina B} and Anett Peters and Gesa Stege and Brix, {Silke R} and Catherine Meyer-Schwesinger and Roman-Ulrich M{\"u}ller and Turner, {Jan Eric} and Steinmetz, {Oliver M} and Gunter Wolf and Stahl, {Rolf A K} and Ulf Panzer",
year = "2013",
month = dec,
day = "1",
doi = "10.1681/ASN.2013020130",
language = "English",
volume = "24",
pages = "1955--65",
journal = "J AM SOC NEPHROL",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "12",

}

RIS

TY - JOUR

T1 - MicroRNA-155 drives TH17 immune response and tissue injury in experimental crescentic GN

AU - Krebs, Christian F

AU - Kapffer, Sonja

AU - Paust, Hans-Joachim

AU - Schmidt, Tilman

AU - Bennstein, Sabrina B

AU - Peters, Anett

AU - Stege, Gesa

AU - Brix, Silke R

AU - Meyer-Schwesinger, Catherine

AU - Müller, Roman-Ulrich

AU - Turner, Jan Eric

AU - Steinmetz, Oliver M

AU - Wolf, Gunter

AU - Stahl, Rolf A K

AU - Panzer, Ulf

PY - 2013/12/1

Y1 - 2013/12/1

N2 - CD4(+) T cells play a pivotal role in the pathogenesis of autoimmune disease, including human and experimental crescentic GN. Micro-RNAs (miRs) have emerged as important regulators of immune cell development, but the impact of miRs on the regulation of the CD4(+) T cell immune response remains to be fully clarified. Here, we report that miR-155 expression is upregulated in the kidneys of patients with ANCA-associated crescentic GN and a murine model of crescentic GN (nephrotoxic nephritis). To elucidate the potential role of miR-155 in T cell-mediated inflammation, nephritis was induced in miR-155(-/-) and wild-type mice. The systemic and renal nephritogenic TH17 immune response decreased markedly in nephritic miR-155(-/-) mice. Consistent with this finding, miR-155-deficient mice developed less severe nephritis, with reduced histologic and functional injury. Adoptive transfer of miR-155(-/-) and wild-type CD4(+) T cells into nephritic recombination activating gene 1-deficient (Rag-1(-/-)) mice showed the T cell-intrinsic importance of miR-155 for the stability of pathogenic TH17 immunity. These findings indicate that miR-155 drives the TH17 immune response and tissue injury in experimental crescentic GN and show that miR-155 is a potential therapeutic target in TH17-mediated diseases.

AB - CD4(+) T cells play a pivotal role in the pathogenesis of autoimmune disease, including human and experimental crescentic GN. Micro-RNAs (miRs) have emerged as important regulators of immune cell development, but the impact of miRs on the regulation of the CD4(+) T cell immune response remains to be fully clarified. Here, we report that miR-155 expression is upregulated in the kidneys of patients with ANCA-associated crescentic GN and a murine model of crescentic GN (nephrotoxic nephritis). To elucidate the potential role of miR-155 in T cell-mediated inflammation, nephritis was induced in miR-155(-/-) and wild-type mice. The systemic and renal nephritogenic TH17 immune response decreased markedly in nephritic miR-155(-/-) mice. Consistent with this finding, miR-155-deficient mice developed less severe nephritis, with reduced histologic and functional injury. Adoptive transfer of miR-155(-/-) and wild-type CD4(+) T cells into nephritic recombination activating gene 1-deficient (Rag-1(-/-)) mice showed the T cell-intrinsic importance of miR-155 for the stability of pathogenic TH17 immunity. These findings indicate that miR-155 drives the TH17 immune response and tissue injury in experimental crescentic GN and show that miR-155 is a potential therapeutic target in TH17-mediated diseases.

KW - Animals

KW - Cells, Cultured

KW - Disease Models, Animal

KW - Glomerulonephritis

KW - Humans

KW - Immunity, Humoral

KW - Immunophenotyping

KW - Male

KW - Mice

KW - Mice, Congenic

KW - Mice, Inbred C57BL

KW - Mice, Mutant Strains

KW - MicroRNAs

KW - Neutrophils

KW - Spleen

KW - Th17 Cells

U2 - 10.1681/ASN.2013020130

DO - 10.1681/ASN.2013020130

M3 - SCORING: Journal article

C2 - 23949802

VL - 24

SP - 1955

EP - 1965

JO - J AM SOC NEPHROL

JF - J AM SOC NEPHROL

SN - 1046-6673

IS - 12

ER -