• IMMUNE NETWORK
• /
• v.2 no.3
• /
• pp.142-149
• /
• 2002

Background: Our previous study showed that purified protein derivative (PPD)-stimulated pleural mononuclear cells (PMC) from tuberculous pleurisy (Tbp) produced significantly more $IFN-{\gamma}$ (10- to 70-fold) after in vitro PPD stimulation than freshly isolated pleural cells from malignant pleurisy. The present study was designed to determine whether blocking the CD40-CD40 ligand (CD40L) interaction decreases $IFN-{\gamma}$ production by altering IL-12 levels. Methods: IL-12 and $IFN-{\gamma}$ production after neutralizing anti-CD40L antibody treatment was compared to the efficacy of anti-CD80, anti-CD86, and a combination of anti-CD80 and CD86 (CD80+86) monoclonal antibodies (mAb). These activities were measured by enzyme-linked immunosorbent assays (ELISAs) and reverse transcription-polymerase chain reaction (RT-PCR), after in vitro stimulation with PPO antigen (Ag). Results: Neutralization of CD80, CD86 and CD80+86 did not decrease $IFN-{\gamma}$ and IL-12 production in Tbp-PMC, whereas neutralization of CD40L significantly depressed IL-12 p40 and $IFN-{\gamma}$. In addition, neutralization of CD40L completely inhibited IL-12 p40 and $IFN-{\gamma}$ mRNA expression. Conclusion: The CD40-CD40L interaction might play a major role in IL-12 and $IFN-{\gamma}$ production in Tbp-PMC, thus contributing to protective immunity in human tuberculosis.

• Biomedical Science Letters
• /
• v.13 no.4
• /
• pp.325-332
• /
• 2007

Cell-mediated immune response (CMI) is a major immune protective mechanism against tuberculosis (TB) infection. Among several components involved in CMI, recent studies suggest that CD8+ T cells are important in controlling TB infection. In our previous report, we defined four Mycobacterium tuberculosis (MTB) derived epiotpe peptides specific for HLA-A*0201-restricted CD8+ T cells. These four peptides are $PstAl_{75-83}$, $ThyA_{30-38}$, $RpoB_{127-135}$ and $85B_{15-23}$. In this study, these epitope peptides specific CD8+ T cell responses in tuberculous pleurisy were investigated using ex vivo $IFN-\gamma$ elispot assay and intracellular $IFN-\gamma$ staining method. As a result, we observed these epitope peptide specific CD8+ T cell responses are induced in all three patients with tuberculous pleurisy suggesting that CD8+ T cells are involved in protective immune mechanism against MTB infection in tuberculous pleurisy. However, the CMI to mitogens and MTB antigens from pleural fluids of patients with tuberculous pleurisy does not seem to correlate with that from peripheral blood, although the sample size is too small to make any conclusion. In sum, the MHC I restricted CD8+ T cell responses seem to be induced efficiently in the pleural fluids, at the site of TB infection, in which the CMI is actively induced. In addition, these experiments suggest that MHC I restricted CD8+ T cell mediated immune responses are also involved in protective mechanism against MTB infection in extra-pulmonary TB.

• Korean Journal of Veterinary Research
• /
• v.5 no.1
• /
• pp.21-25
• /
• 1965

Throughout the studies the followings were obtained and summarized here. 1. Thickenings of plerua were due to the organized fibrin deposition on the pleural surface. 2. Thickenings of plerura were accompanied with increaseness of fibrous connective tissues in the interlobular and alveolar septa. 3. Eosinophilic inclusions seemed to LCL bodies were observed in the cytoplasms of epithelial cells of bronchi, bronchial glands and in the cytoplasms of mononuclear cells. 4. Histo-pathologically, there were some evidences influenced by viruses and the organisms of Psittacosis-Lymphogranuloma Venereum Group.

• Journal of Veterinary Clinics
• /
• v.20 no.4
• /
• pp.493-495
• /
• 2003

A dead, female, 3 years old, squirrel monkey (Saimiri sciureus) was submitted and examined. Before death the monkey has showed lethargy, recumbency and inappetence since November 14, 2001 and died in November 17. Grossly much fibrin was deposited on the pleura of right lung, pericardium, and diaphragm(pleural part). And reddening of right lung was seen. Histopathologically lung showed severe fibrinous pleuritis, severe edema, thrombosis, and focal necrosis in parenchyma. Also much fibrin and mononuclear cells were deposited on the pericardium. In bacterial culture on the pleura and parenchyma of lung, and pericardium, B. bronchiseptica was isolated. Therefore we confirmed this case as the fatal case by B. bronchiseptica in squirrel monkey.

• Korean Journal of Veterinary Service
• /
• v.30 no.3
• /
• pp.407-414
• /
• 2007

There were eight Korean indigenous cattles affected with bovine tuberculosis (BTB) detected by inspectors at slaughterhouses located in Chungbuk province from May 2006 through July 2007. Postmortem finding of BTB cases was characterized by the presence of several caseous or calcified nodules encapsulated by connective tissue from the pleural/peritoneal surface, livers, lungs and regional lymph nodes On micro-scopic examinations, the characteristic lesion of BTB was the formation granulomatous nodules, which contains central calcified necrotic zone surrounded by epithelioid cells, macrophages and a few Langhans' type giant cells. In addition, mononuclear cells and fibroblasts were also infiltrated. At the periphery, encapsulation was formed that protect the neighboring healthy tissues.

• Tuberculosis and Respiratory Diseases
• /
• v.80 no.1
• /
• pp.77-82
• /
• 2017

Background: Delayed hypersensitivity plays a large role in the pathogenesis of tuberculous pleural effusion (TPE). Macrophages infected with live Mycobacterium tuberculosis (MTB) increase the levels of adenosine deaminase2 (ADA2) in the pleural fluid of TPE patients. However, it is as yet unclear whether ADA2 can be produced by macrophages when challenged with MTB antigens alone. This study therefore evaluated the levels of ADA2 mRNA expression, using monocyte-derived macrophages (MDMs) stimulated with MTB antigens. Methods: Purified monocytes from the peripheral blood mononuclear cells of healthy volunteers were differentiated into macrophages using granulocyte-macrophage colony-stimulating factor (GM-CSF) or macrophage colony-stimulating factor (M-CSF). The MDMs were stimulated with early secretory antigenic target protein 6 (ESAT6) and culture filtrate protein 10 (CFP10). The mRNA expression levels for the cat eye syndrome chromosome region, candidate 1 (CECR1) gene encoding ADA2 were then measured. Results: CECR1 mRNA expression levels were significantly higher in MDMs stimulated with ESAT6 and CFP10, than in the unstimulated MDMs. When stimulated with ESAT6, M-CSF-treated MDMs showed more pronounced CECR1 mRNA expression than GM-CSF-treated MDMs. Interferon-${\gamma}$ decreased the ESAT6- and CFP10-induced CECR1 mRNA expression in MDMs. CECR1 mRNA expression levels were positively correlated with mRNA expression of tumor necrosis factor ${\alpha}$ and interleukin 10, respectively. Conclusion: ADA2 mRNA expression increased when MDMs were stimulated with MTB antigens alone. This partly indicates that pleural fluid ADA levels could increase in patients with culture-negative TPE. Our results may be helpful in improving the understanding of TPE pathogenesis.