Effectors of Th1 and Th17 cells act on astrocytes and augment their neuroinflammatory properties.
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Authors
Prajeeth, Chittappen KKronisch, Julius
Khorooshi, Reza
Knier, Benjamin
Toft-Hansen, Henrik
Gudi, Viktoria
Floess, Stefan
Huehn, Jochen
Owens, Trevor
Korn, Thomas
Stangel, Martin
Issue Date
2017-10-16
Metadata
Show full item recordAbstract
Autoreactive Th1 and Th17 cells are believed to mediate the pathology of multiple sclerosis in the central nervous system (CNS). Their interaction with microglia and astrocytes in the CNS is crucial for the regulation of the neuroinflammation. Previously, we have shown that only Th1 but not Th17 effectors activate microglia. However, it is not clear which cells are targets of Th17 effectors in the CNS. To understand the effects driven by Th17 cells in the CNS, we induced experimental autoimmune encephalomyelitis in wild-type mice and CD4 We observed in α4-deficient mice weak microglial activation but comparable astrogliosis to that of wild-type mice in the regions of the brain populated with Th17 infiltrates, suggesting that Th17 cells target astrocytes and not microglia. In vitro, in response to supernatants from Th1 and Th17 cultures, astrocytes showed altered expression of neurotrophic factors, pro-inflammatory cytokines and chemokines. Furthermore, increased expression of chemokines in Th1- and Th17-treated astrocytes enhanced recruitment of microglia and transendothelial migration of Th17 cells in vitro. Our results demonstrate the delicate interaction between T cell subsets and glial cells and how they communicate to mediate their effects. Effectors of Th1 act on both microglia and astrocytes whereas Th17 effectors preferentially target astrocytes to promote neuroinflammation.Affiliation
HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.PubMed ID
29037246Type
ArticleISSN
1742-2094ae974a485f413a2113503eed53cd6c53
10.1186/s12974-017-0978-3
Scopus Count
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- Creative Commons
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