How the "fever molecule" interacts with its receptors is reported online this week in Nature Immunology. These findings could potentially lead to the development of new anti-inflammatory treatments.
A key inflammatory molecule, interleukin 1 (IL-1), has been called the "fever molecule" because its release triggers increases in body temperature in addition to activating immune cells to fight infection. Prolonged IL-1 exposure can likewise wreak tissue damage, as seen in many autoinflammatory diseases such as rheumatoid arthritis.
Xinquan Wang and colleagues have deduced how IL-1beta, a major form of IL-1, binds to its activating receptor IL-1RI―which promotes inflammation signalling―and inhibitory receptor IL-1RII―which reduces inflammation signaling. Insights from the molecular nature of these interactions could lead to development of compounds that uniquely target IL-1RI but not IL-1RII and thereby function as anti-inflammatory agents.
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