For instance, CIA was markedly suppressed in IL-17-/- mice, and the production of antigen specific T cells and collagen specific immunoglobulin G2a were influenced [34]; IL-1 receptor antagonist-knockout (IL1rn-/-) Toll-like receptor 4-knockout (Tlr4-/-) mice was protected against severe arthritis and had markedly lower numbers of Th17 cells and a reduced capacity to produce IL-17 [35]; Th17 cells predominantly expressed CC chemokine receptor (CCR) 6, and migrated to the inflamed joints [36]. The gene discussed is IL17A; the disease is arthritic joint disease.