Type I interferon response in the central nervous system.
This review is dedicated to the influence of type I IFNs (also called IFN-alpha/beta) in the central nervous system (CNS). Studies in mice with type I IFN receptor or IFN-beta gene deficiency have highlighted the importance of the type I IFN system against CNS viral infections and non-viral autoimmune disorders. Direct antiviral effects of type I IFNs appear to be crucial in limiting early spread of a number of viruses in CNS tissues. Type I IFNs have also proved to be beneficial in autoimmune disorders like multiple sclerosis or experimental autoimmune encephalitis, probably through immunomodulatory effects. Increasing efforts are done to characterize IFN expression and response in the CNS: to identify type I IFN producing cells, to decipher pathways leading to type I IFN expression in those cells, and to identify responding cells. However, reversible and irreversible damages consecutive to chronic exposure of the CNS to type I IFNs underline the importance of a tightly regulated type I IFN homeostasis in this organ.
Paul
Sophie
S
Université catholique de Louvain, Christian de Duve Institute of Cellular Pathology, Microbial Pathogenesis Unit, MIPA-VIRO 74-49, 74, avenue Hippocrate, B-1200, Brussels, Belgium.
Ricour
Céline
C
Sommereyns
Caroline
C
Sorgeloos
Frédéric
F
Michiels
Thomas
T
D000818:Animals; D000998:Antiviral Agents / Q000627:therapeutic use; D001921:Brain / Q000378:metabolism; D002490:Central Nervous System / Q000378:metabolism*; D006801:Humans; D007107:Immune System; D007370:Interferon Type I / Q000378:metabolism*; D016899:Interferon-beta / Q000378:metabolism; D051379:Mice; D008954:Models, Biological; D009474:Neurons / Q000378:metabolism; D053633:Receptor, Interferon alpha-beta / Q000378:metabolism*
D000998:Antiviral Agents; C508032:Ifnar1 protein, mouse; D007370:Interferon Type I; D053633:Receptor, Interferon alpha-beta; D016899:Interferon-beta