NE-κB signaling regulates rnyelination in the CNS

Besides myelination of neuronal axons by oligodendrocytes to facilitate propagation of action potentials, oligodendrocytes also support axon survival and function. A key transcription factor involved in these processes is nuclear factor-kappa B (NF-kappa B), a hetero or homodimer of the Rel family of proteins, including p65, c-Rel, RelB, p50, and p52. Under unstimulated, NE-kappa B remains inactive in the cytoplasm through interaction with NE-kappa B inhibitors (I kappa Bs). Upon activation of NE-kappa B the cytoplasmic I kappa Bs gets degradated, allowing the translocation of NF-kappa B into the nucleus where the dimer binds to the kappa B consensus DNA sequence and regulates gene transcription. In this review we describe how oligodendrocytes are, directly or indirectly via neighboring cells, regulated by NF-kappa B signaling with consequences for innate and adaptive immunity and for regulation of cell apoptosis and survival.