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|Title:||Serum levels of tumor necrosis factor-α, interleukin-1, and interferon- γ in β°-thalassemia/HbE and their clinical significance|
S. N. Wickramasinghe
St Mary's Hospital London
|Keywords:||Biochemistry, Genetics and Molecular Biology;Immunology and Microbiology|
|Citation:||Journal of Interferon and Cytokine Research. Vol.19, No.2 (1999), 105-111|
|Abstract:||Serum levels of tumor necrosis factor-α (TNF-α), interleukin-1α (IL- 1α), and interferon-γ (IFN-γ) were estimated by conventional ELISA kits in 60, 42, and 58 Thai patients, respectively, with β°-thalassemia HbE and found to be above the normal range in 13%, 21%, and 33% of the patients, respectively. Using high-sensitivity ELISA systems, an additional 10 β°- thal/HbE patients were compared with 9 controls for concentrations of circulating TNF-α and IL-1β, and 9 and 5 patients, respectively, but only 1 and none of the controls, respectively, showed values above the normal ranges. In patients with abnormally high IFN-γ levels, basal hemoglobin values were significantly lower than in those with normal levels of the cytokine (mean ± SEM: 6.03 ± 0.24 vs. 7.08 ± 0.18, p < 0.05), although circulating concentrations of soluble transferrin receptors (sTrF) and absolute reticulocyte counts were similar in the two groups. Patients with raised or normal levels of TNF-α, IL-1α, or IL-1β had similar basal hemoglobin values. In a phagocytosis assay, monocytes of patients with raised serum levels of IFN-γ showed significantly more attached or ingested IgG- coated red cells than those of patients with normal concentrations of the cytokine (mean ± SEM: 192 ± 22 vs. 140 ± 14 per 100 monocytes, p < 0.05). Moreover, in 3 of 4 of the former patients, the number of attached or ingested IgG-coated red cells per 100 monocytes was above the 95% reference limit for the latter patients. The results suggest that IFN-γ aggravates the anemia of β°-thal/HbE by activating mononuclear phagocytes for destruction of red cells but not by inhibiting erythropoiesis. The elevated serum levels of TNF-α and IL-1 could contribute to complications of the disease, such as cachexia and thromboembolic phenomena.|
|Appears in Collections:||Scopus 1991-2000|
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