期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 134, 期 2, 页码 366-373出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/jid.2013.334
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类别
资金
- NIH [CA-16042, AI-28697, R01-AR-053542]
- JCCC
- UCLA AIDS Institute
- UCLA School of Medicine
- UCLA Clinical and Translational Science Institute [UL1TR00124]
Acne vulgaris is the most common skin disorder affecting millions of people worldwide and inflammation resulting from the immune response targeting Propionibacterium acnes has a significant role in its pathogenesis. In this study, we have demonstrated that P. acnes is a potent inducer of T helper 17 (Th17) and Th1, but not Th2 responses in human peripheral blood mononuclear cells (PBMCs). P. acnes stimulated expression of key Th17-related genes, including IL-17A, ROR alpha, RORc, IL-17RA, and IL-17RC, and triggered IL-17 secretion from CD4(+), but not from CD8(+) T cells. Supernatants from P. acnes stimulated PBMCs were sufficient to promote the differentiation of naive CD4(+)CD45RA T cells into Th17 cells. Furthermore, we found that the combination of IL-1 beta, IL-6, and transforming growth factor-beta-neutralizing antibodies completely inhibited P. acnes induced IL-17 production. Importantly, we showed that IL-17-expressing cells were present in skin biopsies from acne patients but not from normal donors. Finally, vitamin A (all-trans retinoic acid) and vitamin D (1,25-dihydroxyvitamin D3) inhibited P. acnes induced Th17 differentiation. Together, our data demonstrate that IL-17 is induced by P. acnes and expressed in acne lesions and that both vitamin A and D could be effective tools to modulate Th17-mediated diseases such as acne.
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