Rheumatoid Arthritis (RA) severely impacts the life of affected individuals and current treatments are not effective in all patients. Fibroblast-like synoviocytes (FLS) are joint stromal cells which serve a key role in joint destruction during RA. Therefore, inflammatory mediators promoting FLS-driven joint destruction are considered important drug targets in RA. The group has evidence supporting a previously unrecognized mechanism of FLS activation by group 2 innate lymphoid cells (ILC2s), which challenges the current dogma regarding the role of ILC2 in RA. Thus, the objective is to determine if joint-localized ILC2 play a pathogenic, rather than protective, role in RA by promoting FLS-driven joint damage.