期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 131, 期 9, 页码 1785-1786出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/jid.2011.200
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- NIAMS NIH HHS [P50 AR05508, P50 AR055508, P30 AR039750, R01 AR05498, P30 AR39750, R01 AR051498] Funding Source: Medline
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 ROR gamma t. 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.
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