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Infection and Immunity, August 2000, p. 4477-4484, Vol. 68, No. 8
Department of
Microbiology1 and Department of
Therpeutic Radiology,2 College of Medicine,
Chungnam National University, Taejon 301-131, Department of
Microbiology,3 and Department of
Obstetrics and Gynecology,4 College of
Medicine, Konyang University, Nonsan, Chungnam 320-711, and
Department of Internal Medicine, Catholic University, Taejon
301-723,5 Korea
Received 3 December 1999/Returned for modification 18 February
2000/Accepted 5 May 2000
The secreted 30-kDa antigen (Ag) of Mycobacterium
tuberculosis directly stimulates Th1-type protective cytokine
responses in healthy tuberculin reactors but not in patients with
active tuberculosis (TB). To examine the cytokine profiles attributable to Th1 suppression associated with active TB, interleukin-12 (IL-12), IL-18, and IL-10 production in response to a 30- or 32-kDa Ag in 16 patients with active pulmonary TB and 24 healthy controls was
investigated by enzyme-linked immunosorbent assay. In TB patients, production of IL-12 p40, as well as gamma interferon (IFN-
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Copyright © 2000, American Society for Microbiology. All rights reserved.
Depressed Interleukin-12 (IL-12), but not IL-18,
Production in Response to a 30- or 32-Kilodalton Mycobacterial
Antigen in Patients with Active Pulmonary Tuberculosis
), by 30- or 32-kDa Ag-stimulated peripheral blood mononuclear cells (PBMC) was
significantly decreased compared with that in healthy tuberculin
reactors. There were no significant differences in IL-18 production
between patients and controls early during stimulation (16 h). However,
PBMC from patients showed significantly enhanced IL-18 proteins after
96 h of stimulation. Similarly, higher IL-10 production was
observed in the TB patients than in healthy tuberculin reactors. After
2 months of anti-TB therapy, the mean IFN-
and IL-12 p40 production
and the mean blastogenic responses were significantly increased in PBMC
in the 10 TB patients who were followed up. Our findings provide
evidence that depressed IL-12 in response to the 30- or 32-kDa Ag is
involved in the immunopathogenesis of human active pulmonary TB.
*
Corresponding author. Mailing address: Department of
Microbiology, School of Medicine, Chungnam National University, 6 Munhwa-dong, Chung-ku, Taejon 301-131, Korea. Phone: 82-42-580-8243. Fax: 82-42-585-3686. E-mail:
hayoungj{at}hanbat.chungnam.ac.kr.
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