Publication: Intracellular production of type I and type II cytokines during HIV-1 progression in Thai patients
Issued Date
2003-03-01
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ISSN
0125877X
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2-s2.0-0042122370
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Mahidol University
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SCOPUS
Bibliographic Citation
Asian Pacific Journal of Allergy and Immunology. Vol.21, No.1 (2003), 43-48
Suggested Citation
Nattawat Onlamoon, Surada Lerdwana, Winai Ratanasuwan, Surapol Suwanagool, Pilaipan Puthavathana, Kovit Pattanapanyasat Intracellular production of type I and type II cytokines during HIV-1 progression in Thai patients. Asian Pacific Journal of Allergy and Immunology. Vol.21, No.1 (2003), 43-48. Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/20919
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Title
Intracellular production of type I and type II cytokines during HIV-1 progression in Thai patients
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Abstract
A type I to type II cytokine switch on cells of the immune system has been suggested as a critical step in the etiology of HIV infection. In this study, type I and type II cytokine production of both CD4+ and CD8+ T cells activated by superantigen were investigated in 10 healthy donors and 39 HIV-I infected patients. Patients were divided into 3 groups based on their CD4 count (< 200, 200-500, > 500 cells/μl). Whole blood from each subject was activated by staphylococcal enterotoxin B (SEB) and anti-CD28. Intracellular cytokine stainings for proinflamatory cytokine (TNF-α), type I cytokines (IFN-γ and IL-2) and type II cytokines (IL-4 and IL-5) in CD4+ and CD8+ T lymphocytes were determined by flow cytometer. Type I cytokine (IFN-γ) expression in CD4+ T cells co-expressing with CD69 were significantly increased in HIV infected patients, particularly in patients with CD4 counts < 200 and 200-500 cells/μl (means ± S.D. of 20.7 ± 18.7% and 10.5 ± 5.9%, respectively) when compared with 4.8 ± 1.8% in the normal group (p < 0.05). But IL-2 production in both groups of patients was significantly lower than the normal (3.8 ± 2.6% and 3.2 ± 1.4% in patients with <200, 200-500 cells/μl, and 5.9 ± 1.5% in the normal group) (p < 0.05). For type II cytokines, there was no difference in all groups of subjects when IL-4 was determined. However, IL-5 production was significantly higher in patients with a CD4 count < 200 cells/μl (0.6 ± 0.5%) than that in the normal group (0.1 ± 0.1%) (p < 0.005). CD8+ T cells also showed higher IFN-γ production in patients with a CD4 count < 200 cells/μl (11.9 ± 4.7%) and 200-500 cells/μl (12.0 ± 4.3%) than the normal group (5.3 ± 2.5%) (p < 0.005). In contrast, IL-2 production in CD8+ T cells was low in these HIV infected patients (0.3 ± 0.2%, 0.3 ± 0.2%, and 0.3 ± 0.4% in patients with < 200, 200-500, and > 500 cells/μl, respectively), which was significantly different compared to the control group (1.2 ± 0.8%) (p < 0.05). For type II cytokines, only IL-4 production in patients with a CD4 count < 200 cells/μl (0.1 ± 0.1%) was significantly reduced when compared to the other groups (p < 0.05). This study shows that although HIV infection alters the production of both type I and type II cytokines, it does not induce a polarized type I or type II state in the course of HIV-1 progression in Thai patients.