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Depressed interleukin-12 production by peripheral blood mononuclear cells after in vitro stimulation with the 30-kDa antigen in recurrent pulmonary tuberculosis patients.

Authors
  • Lee, Ji-Sook
  • Song, Chang-Hwa
  • Kim, Chul-Hee
  • Kong, Suck-Jun
  • Shon, Mal-Hyun
  • Suhr, Ji-Won
  • Jung, Sung-Soo
  • Lim, Jae-Hyun
  • Kim, Hwa-Jung
  • Park, Jeong-Kyu
  • Paik, Tae-Hyun
  • Jo, Eun-Kyeong
Type
Published Article
Journal
Medical microbiology and immunology
Publication Date
May 01, 2003
Volume
192
Issue
2
Pages
61–69
Identifiers
PMID: 12736818
Source
Medline
License
Unknown

Abstract

Some patients develop recurrent tuberculosis (R-TB), even after successfully completing initial anti-tubercular treatment. Although R-TB may be caused by relapse or exogenous reinfection, little is known about the underlying host responses associated with R-TB. This study investigated the profile of cytokines [interferon (IFN)-gamma, interleukin (IL)-12, tumor necrosis factor (TNF)-alpha, IL-6, and IL-10] present in peripheral blood mononuclear cells (PBMCs) of 17 R-TB patients after stimulation with the 30-kDa antigen (Ag) or purified protein derivative (PPD) Ag of Mycobacterium tuberculosis. These data were compared with data obtained from 15 patients with newly diagnosed pulmonary TB (N-TB), 22 patients with treatment failure (TF-TB), and 19 healthy tuberculin reactors (HTR). N-TB and R-TB patients were enrolled in this study within 1 month of beginning anti-tubercular chemotherapy. ELISA results showed that IFN-gamma production following stimulation with the 30-kDa Ag was significantly lower in each group of TB patients than in the HTR controls. In addition, patients with R-TB showed the most significant IL-12 depression among the subject groups after in vitro stimulation with either Ag. Furthermore, a significant decrease in TNF-alpha and IL-10 levels was observed in R-TB patients relative to N-TB patients. However, there was no statistical difference in TNF-alpha and IL-10 production between R-TB patients, TF-TB patients, and HTR controls. Our findings suggest that the underlying mechanisms of cytokine regulation might differ between N-TB and R-TB patients, and that decreased IL-12 production in response to the 30-kDa or PPD Ag might be involved in the immunopathogenesis of human R-TB.

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