Studies using models of experimental autoimmune diseases, including arthritis, diabetes, and experimental autoimmune encephalomyelitis (EAE), have indicated that activation of iNKT cells by OCH ameliorates or prevents these Th1-mediated diseases, which was attributed to its induction of IL-4 and Th2 skewing [9,10,11,12]. This evidence concerns the gene IL4 and arthritic joint disease.