Interleukin-6 blockade modulates monocyte recruitment to protect against diastolic dysfunction associated with inflammatory arthritis

Treatment of arthritic mice with an antibody that blocks IL-6 signalling is effective in preventing functional alterations of the heart, likely consequent to regulation of monocyte recruitment, and reductions in numbers of pro-inflammatory macrophages and fibroblasts. These preclinical data could prompt specific studies to determine the efficacy of anti-IL-6 therapy in patients at increased risk of cardiac alterations that lead to heart failure.