Hilal Bhat, Karl S Lang, Cornelia Hardt, Judith Lang
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引用次数: 6
Abstract
While the role of interferon during systemic disease is well known and its immune modulating functions and its role in antiviral activity were extensively studied, the role of IFN-I in the brain is less clear. Here we summarize the most important literature on IFN in homeostasis of the CNS and induction of an IFN response during viral infection in the brain. Furthermore, we present work on the roles of IFN in the developing brain as well as during inflammation in the brain. Lastly, we aim to enlighten the functions of IFN on the blood-brain barrier as well as circulation and in cognitive and psychological functions and degeneration. In short, CNS astrocytes produce IFN-β, which is of high relevance for homeostasis in the brain. IFN-β regulates phagocytic removal of myelin debris by microglia. IFN-I limits the permeability of the blood-brain barrier. Disruption of the blood-brain barrier facilitates entrance of peripheral lymphocytes and inflammation. Viral infections during vulnerable phases of embryonic development cause severe fetal pathology and debilitating impairments to human infants. The roles of IFN in these scenarios are diverse and include deficits due to overproduction of IFN during the developmental stage of the brain as seems to be the case in pseudo-TORCH2.
期刊介绍:
Neurosignals is an international journal dedicated to publishing original articles and reviews in the field of neuronal communication. Novel findings related to signaling molecules, channels and transporters, pathways and networks that are associated with development and function of the nervous system are welcome. The scope of the journal includes genetics, molecular biology, bioinformatics, (patho)physiology, (patho)biochemistry, pharmacology & toxicology, imaging and clinical neurology & psychiatry. Reported observations should significantly advance our understanding of neuronal signaling in health & disease and be presented in a format applicable to an interdisciplinary readership.