The way in which the inflammatory activity of the cytokine IL-33 is controlled is explained in a paper in Nature Immunology this week. IL-33 plays an important role in inflammatory conditions of the lung, such as asthma and understanding how this pathway is regulated may provide a strategy to ease such inflammatory conditions.
IL-33 mediates its effects exclusively through its receptor ST2L which led Yutong Zhao and colleagues to look at ways in which this interaction could be regulated. They identified an intracellular molecule called FBXL19 which binds directly to ST2L causing it to be degraded, thereby blunting the inflammatory action of IL-33. Loss of FBXL19 exacerbated the symptoms of lung inflammation whereas an overabundance of this molecule dampened inflammation. Because of the widespread expression of ST2L, the authors conclude that FBXL19 likely plays a generalized role in controlling the pro-inflammatory effects of IL-33.
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