Despite the key rolesimportance of Th17 cells in autoimmune diseases, it remains unclear how they control tissue-residentother inflammatory cells in autoimmune tissue damage. Using a mouse model (SKG mice) of spontaneous Th17 cell-mediated autoimmune arthritis, we showed that arthritogenic IL-17-producing Th17 cells stimulated fibroblast-like synoviocytes (FLS) via IL-17 to secrete GM-CSF and also expanded synovial resident innate lymphoid cells (ILCs) in inflamed joints. Activated synovial ILCs, which expressed CD25, IL-33Ra, and TLR9, produced abundant GM-CSF upon stimulation by IL-2, IL-33, or CpG DNA. Loss of GM-CSF production by either ILCs or radio-resistant stromal cells such as FLS prevented Th17 cell-mediated arthritis. In contrast, GM-CSF production by Th17 cells was not mandatory. Together with the presence of GM-CSF-producing ILCs in inflamed joints of rheumatoid arthritis patients, these results indicate that a cellular cascade of autoimmune IL-17-producing Th17, ILCs and non-lymphoid stromal cells, via IL-17 and GM-CSF, mediates chronic joint inflammation and can be a target for therapeutic intervention.