Abstract
Rheumatoid arthritis is characterized by an inflammatory response in synovial joints, showing a predominant influx of neutrophils. A key mediator of the resolution of inflammation and the uptake of apoptotic cells, or efferocytosis, is the receptor tyrosine kinase Mer. Overexpression of the Mer ligand Pros1 resulted in reduced production of inflammatory mediators by macrophages and synovial cells of arthritic mice, diminished joint pathology, reduced numbers of cleaved Caspase 3-positive apoptotic cells and secondary necrotic neutrophils. Conversely, inhibiting Mer‐mediated efferocytosis by either antibodies or Mertk gene ablation resulted in aggravation of arthritis, as evidenced by increased inflammation and tissue destruction. Additionally, Mer‐inhibited mice had increased numbers of apoptotic cells in their joints, and higher serum levels of IL‐16C, a cytokine released by secondary necrotic neutrophils. Together, these results demonstrate that Mer locally plays an exceptional protective role in joint disease by enhancing resolution of arthritis‐associated inflammation.
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