作者
Hans‐Joachim Paust,Ning Song,Donatella De Feo,Nariaki Asada,Selma Tuzlak,Yu Zhao,Jan-Hendrik Riedel,Malte Hellmig,Amirrtavarshni Sivayoganathan,Anett Peters,Anna Kaffke,Alina Borchers,Ulrich Wenzel,Oliver M. Steinmetz,Gisa Tiegs,Elisabeth Meister,Matthias Mack,Christian Kurts,Sibylle von Vietinghoff,Maja T. Lindenmeyer,Elion Hoxha,Rolf A.K. Stahl,Tobias B. Huber,Stefan Bonn,Catherine Meyer-Schwesinger,Thorsten Wiech,Jan‐Eric Turner,Burkhard Becher,Christian F. Krebs,Ulf Panzer
摘要
GM-CSF in glomerulonephritis Despite 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