The production of interferon gamma by peripheral T lymphocytes in patients with allergic asthma upon stimulation with Der p2 antigen.
- Author:
Mi Sun KIM
1
;
Ji Soo LEE
;
Young Joo CHO
Author Information
1. Ewha Womans University College of Medicine, Department of Internal Medicine, Korea. yjcho@mm.ewha.ac.kr
- Publication Type:Original Article
- MeSH:
Asthma*;
Calcium;
Cytokines;
Dermatophagoides pteronyssinus;
Flow Cytometry;
Humans;
Inflammation;
Interferons*;
T-Lymphocytes*
- From:Journal of Asthma, Allergy and Clinical Immunology
2002;22(2):436-445
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: Recently, distinct cytokine-secreting subsets of CD8+ T cells, similar to their CD4+ Th1- and Th2-type counterparts, have been identified. In order to investigate the role of CD8+ T cells in the pathogenesis of allergic asthma, we determined the changes in the proportion of CD3, CD4+ and CD8+ T cells that expressed the IFN-gamma by Dermatophagoides pteronyssinus antigen 2 (Der p2) activation. METHODS: Peripheral blood mononuclear cells (PBMCs) were obtained from mild persistent allergic asthmatic(n=12) and control subjects(n=8) and cultured with Der p2 for 3 days, and then 12-0-tetracanoylphorbol-13-acetate and calcium ionophore were added 4 hours before staining. Surface CD3, CD4 or CD8 with intracytoplasmic IFN-gamma was measured simultaneously by flow cytometry. RESULTS: Comparing asthmatics with control subjects, we found no differences in the percentage of CD3+, CD4+, or CD8+ T cells in PBMCs stimulated with or without Der p2. When PBMCs were cultured in media only, the proportion of cells producing the cytokines IFN-gamma was similar in CD3+, CD4+ cells, but was significantly lower in CD8+ cells of the asthma group compared to the controls. Both CD4+ and CD8+ subsets revealed a similar degree of reduction in IFN-gamma positive cells in the asthma group compared with the controls by the stimulation of Der p2. CONCLUSION: These findings suggest that CD8+ T cells may be important in the pathogenesis of asthmatic inflammation by modulating the production of IFN-gamma.