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T cell chemokine receptors and cytokines in asthma.

Authors :
Cevhertaş, Laçin
Yılmaz, Abdullah
Tahralı, Ilhan
Küçüksezer, Umut Can
Deniz, Günnur
Erten, Gaye
Gemicioğlu, Bilun
Source :
Turkish Journal of Immunology; 2016 Supplement, Vol. 4, p37-37, 1/3p
Publication Year :
2016

Abstract

T cell subgroups are known to play important roles in the pathogenesis of allergic and non-allergic asthma. In this study the expression of the surface markers including CD4, CD8, CCR3, CCR4, CXCR3 and intracytoplasmic cytokine (IFN-g, IL-4 and IL-10) profiles of peripheral blood mononuclear cells in stimulated (PMA/ionomicin) and unstimulated conditions were investigated by flow cytometry. Stimulated Th cells increased their CXCR3+ IFN-g, CXCR3+ IL-4, CCR3+ IFN-g, CCR3+ IL-4, CCR3+ IL-10, CCR4+ IL-10 expressions in allergic asthma; but CXCR3+ IFN-g, CXCR3+ IL-4, CXCR3+ IL-10, CCR3+ IFN-g, CCR3+ IL-4 and CCR3+ IL-10 expression in non-allergic asthma. Cytotoxic T cells in allergic asthma expressed higher CCR3+ IFN-g, CCR3+ IL-4, CCR3+ IL-10, CCR4+ IL-4, CCR4+ IL-10 after stimulation. On the other hand CD8+ CXCR3+ IFN-g and CD8+ CXCR3+ IL-10 expressions increased in non-allergic asthma under the same stimulation. In our study T cells tended to elevate their intracellular cytokine levels in all study groups under both conditions. Comparing patients with allergic and non-allergic asthma, CCR3+ and CCR4+ Type 2 helper T cells produced higher amounts of IL-10 compared to Type 1 CD4+ CXCR3+ cells in allergic asthma. CD4+ CCR4+ cells expressed higher IFN-g and IL-10 levels without any stimulation in patients with allergic and non-allergic asthma respectively. In summary, our results indicate the role of T cells in the pathogenesis of allergic and non-allergic asthma, but also the complexity of the disease which can not be explained by using only the simple Th1/Th2 paradigma. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
1301109X
Volume :
4
Database :
Complementary Index
Journal :
Turkish Journal of Immunology
Publication Type :
Academic Journal
Accession number :
120570803