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Induction of atypical EAE mediated by transgenic production of IL‐6 in astrocytes in the absence of systemic IL‐6
Author(s) -
Giralt Mercedes,
Ramos Raquel,
Quintana Albert,
Ferrer Beatriz,
Erta Maria,
CastroFreire Marco,
Comes Gemma,
Sanz Elisenda,
Unzeta Mercedes,
Pifarré Paula,
García Agustina,
Campbell Iain L.,
Hidalgo Juan
Publication year - 2013
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.22457
Subject(s) - experimental autoimmune encephalomyelitis , astrocyte , biology , immunology , autoimmunity , genetically modified mouse , central nervous system , cerebellum , microglia , transgene , encephalomyelitis , multiple sclerosis , neuroscience , inflammation , immune system , biochemistry , gene
Interleukin (IL)‐6 is crucial for the induction of many murine models of autoimmunity including experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. While IL‐6‐deficient mice (IL‐6 KO) are resistant to EAE, we showed previously that in transgenic mice with astrocyte‐targeted production of IL‐6‐restricted to the cerebellum (GFAP‐IL6), EAE induced with MOG 35–55 was redirected away from the spinal cord to the cerebellum. To further establish the importance of IL‐6 produced in the central nervous system, we have generated mice producing IL‐6 essentially only in the brain by crossing the GFAP‐IL6 mice with IL‐6 KO mice. Interestingly, GFAP‐IL6‐IL‐6 KO mice showed a milder but almost identical phenotype as the GFAP‐IL6 mice, which correlated with a lower load of inflammatory cells and decreased microglial reactivity. These results indicate that not only is cerebellar IL‐6 production and eventual leakage into the peripheral compartment the dominating factor controlling this type of EAE but that it can also facilitate induction of autoimmunity in the absence of normal systemic IL‐6 production. © 2013 Wiley Periodicals, Inc.

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