한빛사 논문
Abstract
Ho-Keun Kwona, Choong-Gu Leea, Jae-Seon Soa, Chang-Suk Chaea, Ji-Sun Hwanga, Anupama Sahooa, Jong Hee Namb, Joon Haeng Rheeb, Ki-Chul Hwangc, and Sin-Hyeog Ima,d,1
aDepartment of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 500-712, Korea;
bChonnam National University Medical School, Gwangju 501-749, Korea;
cCardiovascular Research Institute, Yonsei University College of Medicine, Seoul 120-752, Korea; and
dCenter for Distributed Sensor Network, Gwangju Institute of Science and Technology, Gwangju 500-712, Korea
Abstract
The beneficial effects of probiotics have been described in many diseases, but the mechanism by which they modulate the immune system is poorly understood. In this study, we identified a mixture of probiotics that up-regulates CD4+Foxp3+ regulatory T cells (Tregs). Administration of the probiotics mixture induced both T-cell and B-cell hyporesponsiveness and down-regulated T helper (Th) 1, Th2, and Th17 cytokines without apoptosis induction. It also induced generation of CD4+Foxp3+ Tregs from the CD4+CD25? population and increased the suppressor activity of naturally occurring CD4+CD25+ Tregs. Conversion of T cells into Foxp3+ Tregs is directly mediated by regulatory dendritic cells (rDCs) that express high levels of IL-10, TGF-β, COX-2, and indoleamine 2,3-dioxygenase. Administration of probiotics had therapeutical effects in experimental inflammatory bowel disease, atopic dermatitis, and rheumatoid arthritis. The therapeutical effect of the probiotics is associated with enrichment of CD4+Foxp3+ Tregs in the inflamed regions. Collectively, the administration of probiotics that enhance the generation of rDCs and Tregs represents an applicable treatment of inflammatory immune disorders.
regulatory T cell, inflammation, atopic dermatitis, inflammatory bowel disease, rheumatoid arthritis
Footnotes
1To whom correspondence should be addressed at: Department of Life Sciences, Gwangju Institute of Science and Technology, 1 Oryong-dong, Buk-gu, Gwangju 500-712, Korea.
Author contributions: S.-H.I. designed research; H.-K.K., C.-G.L., J.-S.S., C.-S.C., A.S., J.H.N., and S.-H.I. performed research; J.H.R. contributed new reagents/analytic tools; H.-K.K., J.-S.H., and K.-C.H. analyzed data; and H.-K.K. and S.-H.I. wrote the paper.
The authors declare no conflict of interest.
This article is a PNAS Direct Submission.
This article contains supporting information online at
www.pnas.org/cgi/content/full/0904055107/DCSupplemental.
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