In AIA, IL-23 was required for the development of optimal disease [19]; for CIA, Il23p19−/− mice were completely protected from arthritis, but similar to our findings above with the mBSA/GM-CSF and mBSA/TNF models, mAb inhibition of IL-23 after disease onset was ineffective [20, 21]. This evidence concerns the gene IL37 and arthritic joint disease.