TGF-beta as a promising option in the treatment of multiple sclerosis.
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Heme oxygenase-1 as a target for TGF-β in kidney diseaseThe neuroprotective functions of transforming growth factor beta proteinsInterleukin-35: a Potential Therapeutic Agent for Autoimmune Diseases.TGFβ signaling regulates the timing of CNS myelination by modulating oligodendrocyte progenitor cell cycle exit through SMAD3/4/FoxO1/Sp1.Pilot analysis of cytokines levels in stored granulocyte-colony-stimulating factor-mobilized peripheral blood stem cell concentrates.Inflammation markers in multiple sclerosis: CXCL16 reflects and may also predict disease activityFetuin-A deficiency protects mice from Experimental Autoimmune Encephalomyelitis (EAE) and correlates with altered innate immune response.Ginger extract modulates the expression of IL-12 and TGF-β in the central nervous system and serum of mice with experimental autoimmune encephalomyelitis.Regulatory T-cell as orchestra leader in immunosuppression process of multiple sclerosis.The deviated balance between regulatory T cell and Th17 in autoimmunity.Important roles played by TGF-β in hepatitis B infection.Guard of delinquency? A role of microglia in inflammatory neurodegenerative diseases of the CNS.Interactions of U24 from Roseolovirus with WW domains: canonical vs noncanonical.The role of different subsets of regulatory T cells in immunopathogenesis of rheumatoid arthritisTolerogenic Vaccination with MOG/VitD Overcomes Aggravating Effect of C. albicans in Experimental Encephalomyelitis.The Modulatory Effects of Vitamin D on the Expression of IL-12 and TGF-β in the Spinal Cord and Serum of Mice with Experimental Autoimmune Encephalomyelitis.Direct modulation of myelin-autoreactive CD4+ and CD8+ T cells in EAE mice by a tolerogenic nanoparticle co-carrying myelin peptide-loaded major histocompatibility complexes, CD47 and multiple regulatory molecules.Differentially expressed microRNA in multiple sclerosis: A window into pathogenesis?Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways
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TGF-beta as a promising option in the treatment of multiple sclerosis.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
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scientific article published on 11 March 2009
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
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vědecký článek
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name
TGF-beta as a promising option in the treatment of multiple sclerosis.
@en
TGF-beta as a promising option in the treatment of multiple sclerosis.
@nl
type
label
TGF-beta as a promising option in the treatment of multiple sclerosis.
@en
TGF-beta as a promising option in the treatment of multiple sclerosis.
@nl
prefLabel
TGF-beta as a promising option in the treatment of multiple sclerosis.
@en
TGF-beta as a promising option in the treatment of multiple sclerosis.
@nl
P1433
P1476
TGF-beta as a promising option in the treatment of multiple sclerosis
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P2093
Monireh Mohsenzadegan
P304
P356
10.1016/J.NEUROPHARM.2009.02.007
P577
2009-03-11T00:00:00Z