Astrocyte-immune cell interactions in physiology and pathology

Astrocytes play both physiological and pathological roles in maintaining central nervous system (CNS) function. Here, we review the varied functions of astrocytes how these might change subsets reactive astrocytes. We current understanding astrocyte interactions with microglia vasculature protective barriers as well highlight recent insights into physiologic sub-states identified by transcriptional profiling. Our goal is to stimulate inquiry molecular identifiers link specific functional changes define implications heterogeneous brain function pathology. Defining complex has potential yield new therapies CNS injury, infection, disease. are bushy star-shaped glial cells that, like neurons oligodendrocytes, arise from a radial cell population surrounding ventricular zone early developing (Rowitch Kriegstein, 2010Rowitch D.H. Kriegstein A.R. Developmental genetics vertebrate glial-cell specification.Nature. 2010; 468: 214-222Crossref PubMed Scopus (347) Google Scholar). tile all parts spinal cord parenchyma integral trophic, structural, metabolic development physiology (Molofsky et al., 2012Molofsky A.V. Krencik R. Ullian E.M. Tsai H.H. Deneen B. Richardson W.D. Barres B.A. Rowitch disease: neurodevelopmental perspective.Genes Dev. 2012; 26: 891-907Crossref Scholar; Allen Eroglu, 2017Allen N.J. Eroglu C. Cell Biology Astrocyte-Synapse Interactions.Neuron. 2017; 96: 697-708Abstract Full Text PDF In extreme contexts such inflammation, neurodegenerative disease, acute become “reactive,” undergoing dramatic shifts at morphological, molecular, levels. These rapid alter ability maintain homeostasis can have profound effects on survival recovery other cells. Most descriptions fall three broad classes: those induced response injury (e.g., axotomy), infection and/or some form disease A unifying feature classes that emerge external stimuli. contrast this “disease” could altered transcriptomic, proteomic, features due an inherent disease-causing mutation fibrillary acidic protein [GFAP] mutations Alexander’s disease; Alexander, 1949Alexander W.S. Progressive fibrinoid degeneration associated mental retardation hydrocephalic infant.Brain. 1949; 72: 373-381, 3Crossref (232) Quinlan 2007Quinlan R.A. Brenner M. Goldman J.E. Messing A. GFAP its role Alexander disease.Exp. Res. 2007; 313: 2077-2087Crossref (142) Although it true also react stimuli reactive, themselves not necessarily baseline. An example one encounter reported during diseases amyotrophic lateral sclerosis (ALS). This progressive characterized death upper cortical lower motor neurons, implicated active contributors neurodegeneration. 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