Hydroquinone, a major component in cigarette smoke, reduces IFN-gamma production in antigen-primed lymphocytes
- Authors
- Choi, Jin Myung; Cho, Young-Chang; Cho, Won Jea; Kim, Tae Sung; Kang, Bok Yun
- Issue Date
- 3월-2008
- Publisher
- PHARMACEUTICAL SOC KOREA
- Keywords
- hydroquinone; IFN-gamma; T cell; AP-1; NF-kappa B
- Citation
- ARCHIVES OF PHARMACAL RESEARCH, v.31, no.3, pp.337 - 341
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- ARCHIVES OF PHARMACAL RESEARCH
- Volume
- 31
- Number
- 3
- Start Page
- 337
- End Page
- 341
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/123957
- DOI
- 10.1007/s12272-001-1161-1
- ISSN
- 0253-6269
- Abstract
- Exposure to cigarette smoke is known to suppress immune responses and to increase the incidence and severity of respiratory infections. In this study, we determined the effect of hydroquinone (HQ), which is found at high concentrations in cigarette smoke, on interferon-gamma (IFN-gamma) production by lymphocytes. HQ significantly inhibited IFN-gamma secretion by keyhole limpet hemocyanin-primed lymphocytes in a dose-dependent manner. In addition, HQ inhibited IFN-gamma secretion in effector CD4(+) T cells and Th1-differentiated CD4+ T cells. The mRNA expression of IFN-gamma and the IFN-gamma gene promoter activity were inhibited by HQ. These results suggest that the inhibitory effect of HQ on IFN-gamma secretion may occur at the transcriptional level. Furthermore, the effects of HQ on transcription factors were investigated. HQ inhibited the transcriptional activity of activator protein-1 and nuclear factor-kappa B, which are known to be involved in IFN-gamma transcriptional activation. These findings provide evidence that HQ might suppress immune responses by reducing the production of IFN-gamma and may explain the susceptibility to microbial infections caused by cigarette smoking.
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Collections - Graduate School > Department of Life Sciences > 1. Journal Articles
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