Thus, it appears that γδ T cell responses in arthritis are dependent, upon non TCR driven mechanisms, including cytokines (IL-1, IL-23, and IL-28) and chemokines affecting homing to the synovium, although a specific contribution of certain antigen selected γδ T cells (e.g., Vγ4Vδ4+ T cells) may also play a role. This evidence concerns the gene IL1B and Arthritis.