Lipoteichoic Acid Suppresses Effector T Cells Induced by <i>Staphylococcus aureus</i>-Pulsed Dendritic Cells
- Authors
- Son, Young Min; Song, Ki-Duk; Park, Sung-Moo; Han, Seung Hyun; Yun, Cheol-Heui
- Issue Date
- Jul-2013
- Publisher
- KOREAN SOC MICROBIOLOGY & BIOTECHNOLOGY
- Keywords
- Lipoteichoic acid; immune tolerance; regulatory T cells; effector CD4(+) T cells; TGF-beta
- Citation
- JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY, v.23, no.7, pp 1023 - 1030
- Pages
- 8
- Journal Title
- JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY
- Volume
- 23
- Number
- 7
- Start Page
- 1023
- End Page
- 1030
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/72119
- DOI
- 10.4014/jmb.1302.02009
- ISSN
- 1017-7825
1738-8872
- Abstract
- Lipoteichoic acid (LTA), uniquely expressed on gram-positive bacteria, is recognized by Toll-like receptor 2 (TLR2) on not only antigen-presenting cells but also activated T cells. Therefore, it is reasonable to assume that LTA is acting on T cells. However, little is known about the effect of LTA on T-cell regulation. In the present study, we investigated the immunomodulatory effects of LTA on CD4(+) T cells. Effector CD4(+) T cells, induced after co-culture with S. aureus-pulsed dendritic cells, produced high levels of interferon-gamma, CD25, CD69, and TLRs 2 and 4. When effector CD4(+) T cells were treated with LTA, the expressions of the membrane-bound form of transforming growth factor (TGF)-beta and forkhead box P3 increased. Coincidently, the proliferation of effector CD4(+) T cells was declined after LTA treatment. When TGF-beta signaling was blocked by the TGF-beta receptor 1 kinase inhibitor, LTA failed to suppress the proliferation of effector CD4(+) T cells. Therefore, the present results suggest that LTA suppresses the activity of effector CD4(+) T cells by enhancing TGF-beta production.
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Collections - College of Biotechnology & Natural Resource > Department of Systems Biotechnology > 1. Journal Articles
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