0000000000126152

AUTHOR

Günter Steiner

showing 1 related works from this author

A T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis.

2017

Multiple sclerosis (MS) is a human neurodegenerative disease characterized by the invasion of autoreactive T cells from the periphery into the CNS. Application of pan-histone deacetylase inhibitors (HDACi) ameliorates experimental autoimmune encephalomyelitis (EAE), an animal model for MS, suggesting that HDACi might be a potential therapeutic strategy for MS. However, the function of individual HDAC members in the pathogenesis of EAE is not known. In this study we report that mice with a T cell-specific deletion of HDAC1 (using the Cd4-Cre deleter strain; HDAC1-cKO) were completely resistant to EAE despite the ability of HDAC1cKO CD4+ T cells to differentiate into Th17 cells. RNA sequencin…

0301 basic medicineReceptors CCR6Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisReceptors CCR4T cellImmunologyCCR4Histone Deacetylase 1C-C chemokine receptor type 6Biologymedicine.disease_causeAutoimmunity03 medical and health sciencesChemokine receptorMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsHumansCells CulturedMice KnockoutChimeraMultiple sclerosisExperimental autoimmune encephalomyelitisGene targetingmedicine.diseaseMolecular biologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureSTAT1 Transcription FactorCancer researchTh17 Cells030215 immunologyJournal of autoimmunity
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