TrbK controls astrocyte-driven oligodendrocyte copper poisoning.

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) associated with the destruction of oligodendrocyte-produced myelin, which results in neuron and oligodendrocyte loss (1, 2). The dysregulated activity of cells of the adaptive immune system, specifically T cells and B cells, plays an important role in MS pathology, particularly during the relapsing–remitting phase of the disease. However, innate immune chronic inflammation driven by CNS-resident cells and recruited monocytes is thought to drive CNS pathology in the progressive phase of MS, an MS phase characterized by the progressive and irreversible accumulation of neurologic disability largely unresponsive to available therapeutic approaches (1, 2). Astrocytes are the most abundant glial cells in the CNS, with important functions in health and disease. In the context of health, astrocytes participate in the development and functional regulation of synapses and the blood–brain barrier, the metabolic support of neurons, and the production of neurotrophic factors (3, 4). During neurologic diseases many of these homeostatic astrocyte functions are impaired, and astrocytes promote CNS pathology through … [↵][1]1To whom correspondence may be addressed. Email: fquintana{at}bwh.harvard.edu or hweiner{at}rics.bwh.harvard.edu. [1]: #xref-corresp-1-1