How immune cells turn off proinflammatory signaling is described in an online paper in Nature Immunology. These findings have implications in understanding the molecular basis by which the cancer-causing virus HTLV-1 can trigger T cell leukemia.
Inflammatory signaling pathways are tightly regulated as prolonged activation can cause tissue damage and is linked to the development of autoimmune diseases, such as rheumatoid arthritis, and some cancers, including colon cancers.
Edward Harhaj and colleagues show that the protein TAX1BP1 is crucial for formation of an intracellular protein complex that acts as a shut-off valve, stopping production of inflammatory mediators. The off-switch is triggered by kinase IKKalpha phosphorylation of TAX1BP1, which allows for the protein’s interaction with other components of the A20 editing complex that act to dissemble proinflammatory signaling platform.
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