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Significance Joint inflammation is the defining characteristic of the autoimmune disease rheumatoid arthritis. Here we use experimental systems to show that the Th2 cytokine IL-4 suppresses the neutrophil potential of causing acute joint inflammation, including suppressing their migration to the inflamed joint, and by upregulating their expression of the inhibitory IgG Fc receptor. We also identify that the pathway is regulated by colony stimulating factor 3. Identifying strategies for early intervention in patients before they develop chronic, debilitating disease is a key focus of the current research in autoimmune diseases. Our study identifies mechanisms that could be exploited therapeutically in patient groups where IgG autoantibodies and neutrophils are thought to play an important role in the pathology.

IL-4 controls activated neutrophil FcγR2b expression and migration into inflamed joints