科研之友
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摘要
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.
- 出版日期2011-9
