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Dysregulated Production of IFN-${gamma}$, IL-12, and IL-10 by Peripheral Blood Mononuclear Cells from Early Active Pulmonary and Multidrug-Resistant Tuberculosis Patients
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  • Dysregulated Production of IFN-${gamma}$, IL-12, and IL-10 by Peripheral Blood Mononuclear Cells from Early Active Pulmonary and Multidrug-Resistant Tuberculosis Patients
  • Dysregulated Production of IFN-${gamma}$, IL-12, and IL-10 by Peripheral Blood Mononuclear Cells from Early Active Pulmonary and Multidrug-Resistant Tuberculosis Patients
저자명
Lee. Ji-Sook,Son. Hee-Sook,Song. Chang-Hwa,Kim. Hwa-Jung,Park. Jeong-Kyu,Paik. Tae-Hyun,Suhr. Ji-Won,Kim. Chul-Hee,Kong. Suck-Ju
간행물명
Journal of bacteriology and virology : JBV
권/호정보
2002년|32권 2호|pp.211-219 (9 pages)
발행정보
대한미생물학회
파일정보
정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

In this study, we investigated profiles of the cytokines IFN-${gamma}$, IL-12, and IL-10 in active pulmonary tuberculosis (EAPTB) patients, HIV-negative patients with multidrug-resistant tuberculosis (MDR-TB) and in healthy tuberculin reactors (HTR). We studied the responses of peripheral blood mononuclear cells (PBMC) from 12 EAPTB patients and 15 MDR-TB patients to stimulation with a purified protein derivatives (PPD) antigen (Ag), and compared them with those from 14 HTR. Using ELISA, IFN-${gamma}$ production was found to be significantly depressed, while IL-10 was significantly elevated in both MDR-TB and EAPTB after in vitro stimulation with PPD, compared with those in HTR. Although there was no significant difference in IL-12 production among the three groups, mean IL-12 production was highest in patients with MDR-TB. In these patients, IL-12 production was significantly correlated with IL-10 expression, but not IFN-${gamma}$ production. In addition, neutralization of endogenous IL-10 led to enhanced IFN-${gamma}$ and IL-$12R{eta}2$ mRNA expression in TB patients. Our findings suggest that both groups of TB patients may have a similar disregulated pattern of IL-12, IL-10, and IFN-${gamma}$ production during M. tuberculosis infection. Furthermore, the results suggest a potentially pathogenic role for IL-10 in impaired Th1 immune responses in TB patients.