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