CSF2 and arthritic joint disease: ILCs with a similar phenotype were also present in normal joints and expanded in collagen antibody-induced arthritis in C57/BL6 mice, indicating that the presence and expansion of GM-CSF-producing synovial ILCs was not dependent on the mouse genetic background or the mode of arthritis induction by autoimmune Th17 cells or autoantibody (Figures 4K and S4).