Taken together, while clearly demonstrating involvement of γδ T cells in experimental arthritis, these data highlight the need to dissect subsets of γδ T cells when analyzing their role in pathogenesis of antigen induced arthritis in mice, while supporting the idea that their role is not directly associated with a direct response to the instigating antigen, but rather is related to effector mechanisms such as IL-23 induced production of IL-17 at the site of inflammation. This evidence concerns the gene IL17A and Arthritis.