CD4 + T cells produce GM-CSF and drive immune-mediated glomerular disease by licensing monocyte-derived cells to produce MMP12.
Hans-Joachim PaustNing SongDonatella De FeoNariaki AsadaSelma TuzlakYu ZhaoJan-Hendrik RiedelMalte HellmigAmirrtavarshni SivayoganathanAnett PetersAnna KaffkeAlina BorchersUlrich O WenzelOliver M SteinmetzGisa TiegsElisabeth MeisterMatthias MackChristian KurtsSibylle von VietinghoffMaja T LindenmeyerElion HoxhaRolf A K StahlTobias B HuberStefan BonnCatherine Meyer-SchwesingerThorsten WiechJan-Eric TurnerBurkhard BecherChristian F KrebsUlf PanzerPublished in: Science translational medicine (2023)
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.