Blocking the protein interferon regulatory factor 5 (IRF5) would significantly reduce inflammation in certain chronic conditions, providing a more specific and effective treatment for patients, as well as fewer side effects from long-term use of current options.
Macrophages and neutrophils, two types of white blood cells, are the most abundant inflammatory cells in diseases driven by inflammation, like rheumatoid arthritis and acute lung injury. Each cell type can play opposing roles, with some macrophages increasing inflammation whilst other macrophages are helping to decrease it. Reducing the presence of these cells in inflamed areas, or switching their function to a ‘repair’ one, typically leads to profound therapeutic benefit.
IRF5 is very important in defining which role macrophages will play, as well as in neutrophil recruitment to affected areas, namely on acute lung injury, making it a great target for new therapies.
Kennedy researcher Miriam Weiss said: "These data highlight IRF5 as a very interesting drug target to treat inflammatory diseases such as rheumatoid arthritis. The next step will be to find ways to block this pathway, so we can move closer to an effective therapy."
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Image: neutrophils detected within the synovial capsule of inflamed knees. Left: control group; right: blocking IRF5.