Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis.

Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis. Research Abstract Details 

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Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis. Abstract Text:

Jian Luo,Peggy P Ho,Marion S Buckwalter,Tiffany Hsu,Lowen Y Lee,Hui Zhang,Dae-Kee Kim,Seong-Jin Kim,Sanjiv S Gambhir,Lawrence Steinman,Tony Wyss-Coray,Jian Luo,Peggy P Ho,Marion S Buckwalter,Tiffany Hsu,Lowen Y Lee,Hui Zhang,Dae-Kee Kim,Seong-Jin Kim,Sanjiv S Gambhir,Lawrence Steinman,Tony Wyss-Coray,

Autoimmune encephalomyelitis, a mouse model for multiple sclerosis, is characterized by the activation of immune cells, demyelination of axons in the CNS, and paralysis. We found that TGF-beta1 synthesis in glial cells and TGF-beta-induced signaling in the CNS were activated several days before the onset of paralysis in mice with autoimmune encephalomyelitis. While early production of TGF-beta1 was observed in glial cells TGF-beta signaling was activated in neurons and later in infiltrating T cells in inflammatory lesions. Systemic treatment with a pharmacological inhibitor of TGF-beta signaling ameliorated the paralytic disease and reduced the accumulation of pathogenic T cells and expression of IL-6 in the CNS. Priming of peripheral T cells was not altered, nor was the generation of TH17 cells, indicating that this effect was directed within the brain, yet affected the immune system. These results suggest that early production of TGF-beta1 in the CNS creates a permissive and dangerous environment for the initiation of autoimmune inflammation, providing a rare example of the brain modulating the immune system. Importantly, inhibition of TGF-beta signaling may have benefits in the treatment of the acute phase of autoimmune CNS inflammation.

Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis. Publishing Authors By Initials

J Luo,PP Ho,MS Buckwalter,T Hsu,LY Lee,H Zhang,DK Kim,SJ Kim,SS Gambhir,L Steinman,T Wyss-Coray,J Luo,PP Ho,MS Buckwalter,T Hsu,LY Lee,H Zhang,DK Kim,SJ Kim,SS Gambhir,L Steinman,T Wyss-Coray,

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Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of clinical investigation

VOLUME: 117

Page Numbers: 3306-15

Journal Abbreviation: J. Clin. Invest.

ISSN: 0021-9738

DAY: 2

MONTH: Nov

YEAR: 2007

Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis. Information

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LANGUAGE: eng

NlmUniqueID: 7802877

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Grant and Affiliation Information for Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis.

AFFILIATION: Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305-5235, USA.

Country: United States

AGENCY: United States NCI

GRANT: CA114747 ICMIC P5

ACRONYM: CA

MEDLINETA: J Clin Invest

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