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Nature Immunology

August 30, 2010

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.

DOI:10.1038/ni.1925 | Original article

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