A prominent feature was down-regulation of gene expression of a number of RA- and CIA-associated Th1 cytokines including IL-17A, IL-23 and CSF-2 indicating that the increased arthritis disease was not driven by development of autoreactive Th17 cells and an enhanced Th17 response28.This interesting observation was further validated by immunohistochemical analysis of inflamed paws of CIA mice showing a significant lower accumulation of IL17-producing CD4 cells in the inflamed area in the CD163−/− mice compared to CD163+/+ mice (Supplementary Fig.S1; p = 0.011). The gene discussed is CD163; the disease is arthritic joint disease.