Functional and genetic assessment of IFN-γ receptor in patients with clinical tuberculosis
Abstract:OBJECTIVE: The molecular basis of the genetic vulnerability underlying the most common form of clinical tuberculosis (TB) remains largely unknown. We speculated that mild genetic defects in the interferon-gamma (IFN-γ) signalling pathway caused a subtle functional impairment of IFN-γ which would explain susceptibility to Mycobacterium tuberculosis in clinical TB.
DESIGN: A case-control study.
RESULTS: We evaluated functional responsiveness to IFN-γ in monocytes from patients with clinical TB (n = 10), and analysed the genetic sequences of the IFN-γ receptor 1 (IFN-γR1) and STAT1 genes in patients with disseminated TB (n = 18). IFN-γ stimulated an increase in the expression of HLA-DR and CD64 on monocytes of both controls and patients; the rate of increase in expression was the same in both groups. Treatment with IFN-γ before lipopolysaccharide (LPS) stimulation further increased tumour necrosis factor-alpha (TNF-α) production as compared to TNF-α production with LPS stimulation alone; the rate of increase in TNF-α production was the same in both groups. The known mutations in the coding sequences of the IFN-γR1 and STAT1 genes were not found in the patients with disseminated tuberculosis.
CONCLUSION: These results suggest that impairment of the IFN-γ signalling pathway did not account for cases of clinical TB in this study.
Document Type: Regular Paper
Affiliations: 1: Department of Internal Medicine, Gachon Medical School, Gil Medical Centre, Incheon, South Korea 2: Department of Clinical Pathology, Gachon Medical School, Gil Medical Centre, Incheon, South Korea 3: Divison of Biological Science, Department of Molecular Biology, Gachon Medical School, Gil Medical Centre, Incheon, South Korea
Publication date: 2004-10-01
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