title: The dark side of regulatory T cells in psoriasis.
abstract: Psoriasis is a hereditary disease elicited by chronic activation of cutaneous T cells. Delineating the mechanistic interplay of the cell subsets involved is key to developing the next generation of effective treatments. In this issue, Bovenschen et al. report that regulatory T cells maintain a fine balance between the transcription factors Foxp3 and RORγt. In patients with psoriasis, Tregs readily turn into IL-17-expressing cells, thus potentially perpetuating the inflammatory process that characterizes the disease. Results demonstrating that the histone/protein deacetylation inhibitor trichostatin A can block this conversion suggest that an epigenetic modification may underlie regulatory T-cell plasticity.
authors.affiliation: Department of Dermatology, Case Western Reserve University, University Hospitals Case Medical Center, Cleveland, Ohio 44106, USA.
authors.forename: David C
authors.initials: DC
authors.lastname: Soler
authors.forename: Thomas S
authors.initials: TS
authors.lastname: McCormick
mesh_terms: D051858:Forkhead Transcription Factors / Q000276:immunology*; D006801:Humans; D020381:Interleukin-17 / Q000276:immunology*; D011565:Psoriasis / Q000276:immunology* / Q000473:pathology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D058504:Th17 Cells / Q000276:immunology*
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C508717:IL17A protein, human; D020381:Interleukin-17