Reciprocal cross‐talk between RANKL and interferon‐γ–inducible protein 10 is responsible for bone‐erosive experimental arthritis

Abstract

Our findings suggest that IP-10 plays a critical role in the infiltration of CD4+ T cells and F4/80+ macrophages into inflamed joints and causes bone destruction. Our results provide the first evidence that IP-10 contributes to the recruitment of inflammatory cells and is involved in bone erosion in inflamed joints.