CD4+ T cells produce GM-CSF and drive immune-mediated glomerular disease by licensing monocyte-derived cells to produce MMP12

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CD4+ T cells produce GM-CSF and drive immune-mediated glomerular disease by licensing monocyte-derived cells to produce MMP12. / Paust, Hans-Joachim; Song, Ning; De Feo, Donatella; Asada, Nariaki; Tuzlak, Selma; Zhao, Yu; Riedel, Jan-Hendrik; Hellmig, Malte; Sivayoganathan, Amirrtavarshni; Peters, Anett; Kaffke, Anna; Borchers, Alina; Wenzel, Ulrich O; Steinmetz, Oliver M; Tiegs, Gisa; Meister, Elisabeth; Mack, Matthias; Kurts, Christian; von Vietinghoff, Sibylle; Lindenmeyer, Maja T; Hoxha, Elion; Stahl, Rolf A K; Huber, Tobias B; Bonn, Stefan; Meyer-Schwesinger, Catherine; Wiech, Thorsten; Turner, Jan-Eric; Becher, Burkhard; Krebs, Christian F; Panzer, Ulf.

in: SCI TRANSL MED, Jahrgang 15, Nr. 687, eadd6137, 15.03.2023.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

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@article{53b64ff7260d44e093973a6e67a4aaa6,
title = "CD4+ T cells produce GM-CSF and drive immune-mediated glomerular disease by licensing monocyte-derived cells to produce MMP12",
abstract = "GM-CSF in glomerulonephritisDespite glomerulonephritis being an immune-mediated disease, the contributions of individual immune cell types are not clear. To address this gap in knowledge, Paust et al. characterized pathological immune cells in samples from patients with glomerulonephritis and in samples from mice with the disease. The authors found that CD4+ T cells producing granulocyte-macrophage colony-stimulating factor (GM-CSF) licensed monocytes to promote disease by producing matrix metalloproteinase 12 and disrupting the glomerular basement membrane. Targeting GM-CSF to inhibit this axis reduced disease severity in mice, implicating this cytokine as a potential therapeutic target for patients with glomerulonephritis. -CM.",
keywords = "Mice, Animals, Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology, Monocytes/metabolism, Matrix Metalloproteinase 12/metabolism, CD4-Positive T-Lymphocytes, Glomerulonephritis/metabolism",
author = "Hans-Joachim Paust and Ning Song and {De Feo}, Donatella and Nariaki Asada and Selma Tuzlak and Yu Zhao and Jan-Hendrik Riedel and Malte Hellmig and Amirrtavarshni Sivayoganathan and Anett Peters and Anna Kaffke and Alina Borchers and Wenzel, {Ulrich O} and Steinmetz, {Oliver M} and Gisa Tiegs and Elisabeth Meister and Matthias Mack and Christian Kurts and {von Vietinghoff}, Sibylle and Lindenmeyer, {Maja T} and Elion Hoxha and Stahl, {Rolf A K} and Huber, {Tobias B} and Stefan Bonn and Catherine Meyer-Schwesinger and Thorsten Wiech and Jan-Eric Turner and Burkhard Becher and Krebs, {Christian F} and Ulf Panzer",
year = "2023",
month = mar,
day = "15",
doi = "10.1126/scitranslmed.add6137",
language = "English",
volume = "15",
journal = "SCI TRANSL MED",
issn = "1946-6234",
publisher = "AMER ASSOC ADVANCEMENT SCIENCE",
number = "687",

}

RIS

TY - JOUR

T1 - CD4+ T cells produce GM-CSF and drive immune-mediated glomerular disease by licensing monocyte-derived cells to produce MMP12

AU - Paust, Hans-Joachim

AU - Song, Ning

AU - De Feo, Donatella

AU - Asada, Nariaki

AU - Tuzlak, Selma

AU - Zhao, Yu

AU - Riedel, Jan-Hendrik

AU - Hellmig, Malte

AU - Sivayoganathan, Amirrtavarshni

AU - Peters, Anett

AU - Kaffke, Anna

AU - Borchers, Alina

AU - Wenzel, Ulrich O

AU - Steinmetz, Oliver M

AU - Tiegs, Gisa

AU - Meister, Elisabeth

AU - Mack, Matthias

AU - Kurts, Christian

AU - von Vietinghoff, Sibylle

AU - Lindenmeyer, Maja T

AU - Hoxha, Elion

AU - Stahl, Rolf A K

AU - Huber, Tobias B

AU - Bonn, Stefan

AU - Meyer-Schwesinger, Catherine

AU - Wiech, Thorsten

AU - Turner, Jan-Eric

AU - Becher, Burkhard

AU - Krebs, Christian F

AU - Panzer, Ulf

PY - 2023/3/15

Y1 - 2023/3/15

N2 - GM-CSF in glomerulonephritisDespite glomerulonephritis being an immune-mediated disease, the contributions of individual immune cell types are not clear. To address this gap in knowledge, Paust et al. characterized pathological immune cells in samples from patients with glomerulonephritis and in samples from mice with the disease. The authors found that CD4+ T cells producing granulocyte-macrophage colony-stimulating factor (GM-CSF) licensed monocytes to promote disease by producing matrix metalloproteinase 12 and disrupting the glomerular basement membrane. Targeting GM-CSF to inhibit this axis reduced disease severity in mice, implicating this cytokine as a potential therapeutic target for patients with glomerulonephritis. -CM.

AB - GM-CSF in glomerulonephritisDespite glomerulonephritis being an immune-mediated disease, the contributions of individual immune cell types are not clear. To address this gap in knowledge, Paust et al. characterized pathological immune cells in samples from patients with glomerulonephritis and in samples from mice with the disease. The authors found that CD4+ T cells producing granulocyte-macrophage colony-stimulating factor (GM-CSF) licensed monocytes to promote disease by producing matrix metalloproteinase 12 and disrupting the glomerular basement membrane. Targeting GM-CSF to inhibit this axis reduced disease severity in mice, implicating this cytokine as a potential therapeutic target for patients with glomerulonephritis. -CM.

KW - Mice

KW - Animals

KW - Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology

KW - Monocytes/metabolism

KW - Matrix Metalloproteinase 12/metabolism

KW - CD4-Positive T-Lymphocytes

KW - Glomerulonephritis/metabolism

U2 - 10.1126/scitranslmed.add6137

DO - 10.1126/scitranslmed.add6137

M3 - SCORING: Journal article

C2 - 36921033

VL - 15

JO - SCI TRANSL MED

JF - SCI TRANSL MED

SN - 1946-6234

IS - 687

M1 - eadd6137

ER -