Taken together with our previous work13, this study provides new evidence that TIARP plays a key role as a negative regulator by suppressing not only activated macrophages, but also cross-talk between infiltrating neutrophils and proliferated FLS via CXCL2/CXCR2 and IL-6, in the pathogenesis of arthritis. This evidence concerns the gene CXCL2 and arthritic joint disease.