Although IL1R2 was highly expressed in neutrophils, IL1R2 knockout did not affect this cell type in mice, suggesting that IL1R2 is not functional in neutrophils.24 In contrast, IL1R2 on macrophages mainly acts as a decoy receptor for IL1.25 The immunosuppressive role of IL1R2 was demonstrated in several studies in vivo, including in chronic skin inflammation, arthritis, endometriosis and autoimmune myocarditis.8 Soluble IL1R2 was also shown to increase in multiple sclerosis patients and was negatively correlated with the severity of the disease.26 The gene discussed is IL1A; the disease is arthritic joint disease.