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DAP12 (also called KARAP) is a transmembrane adapter well known for its role in transducing activation signals for an extended array of receptors in NK cells, granulocytes, monocytes/macrophages, and DCs (1, 2). In this issue of the JCI, Takai and colleagues unveil that DAP12-deficient mice exhibit osteopetrosis and demyelinization of the CNS (3). Human studies have concurrently shown that genetic defects of DAP12 result in a rare syndrome characterized by bone cysts and presenile dementia (4, 5). Thus, DAP12 appears to be critically involved in bone modeling and brain myelination. If so, how can DAP12 regulate both immune and non-immune functions?

DAP12 signaling: from immune cells to bone modeling and brain myelination