Abstract
The changing states of T cell populations responsible for the chronic course of allergic inflammation and diseases, including allergic bronchial asthma, are not yet sufficiently characterized. The aim of this study was to detect phenotypic changes in the CD45RA/CD45RO positive T lymphocytes and the level of regulatory cytokines (TNFα, IFNγ, IL-4, IL-6, IL-8, IL-10, IL-13, IL-17А, IL-17F) in allergic respiratory diseases (ARD) in children. In blood of 90 children aged 3-11 (60 children with ARD and 30 healthy peers) were studied of the immune cellular populations and cytokine indices. The levels of IL-4, IL-8, IL-10, IL-13, IL-17A and IL-17F in blood serum of children with bronchial asthma and allergic rhinitis differed from appropriate indices in control group (p = 0.001). The quantity of CD3+CD8+CD45RACD45RO+cells, T helpers (p < 0.05) and Th effectors simultaneously expressing both isoforms of the CD45RA+and CD45RO receptor in peripheral blood of children with ARD significantly exceeded those in control group (p < 0.001). In healthy children, Th17 population (CD3+CD4+CD196 lymphocytes) comprised 9.49±1.6% of CD3+CD4+of cells, the number of such lymphocytes was significantly increased to 14.5±0.77 in children with allergic diseases (p < 0.001). Absolute numbers of Th17+ cells were 93.0±9.30 and 127,0±72.0 cells/µl respectively (p = 0.002). Indicators of CD4CD45RO positive memory cells in children with ARD was determined as significantly lower (p < 0.001), whereas quantity of CD3+CD19+proved to be higher (p < 0.05) than in healthy peers. Absolute counts of these cells did not differ between the groups. The number of CD8+CD45RO+T lymphocytes was significantly higher in children with allergic diseases (p < 0.025). This research shows that the quantitative ratio of CD3+CD8+CD45RA+and CD3+CD8+CD45RO+populations of T cells, and increased levels of cytokines, synthesizable via Th2 and Th17, in peripheral blood may be helpful for understanding genesis of allergic respiratory diseases, and extends our knowledge on immune mechanisms of allergic disorders for individualization of therapeutic programs.
Highlights
In case of allergic diseases, imbalance in regulation of immune response to antigen is accompanied by decrease of suppressive activity of regulatory T cells, production of specific immunoglobulin antibodies IgE or implementation of delayed-type hypersensitivity reaction and allergic inflammation
CD3+CD4+ populations (Th1, Th2, Th9, Th17, Th22, Treg and Tfh), CD3+CD8+ of memory and effector subpopulations differ on extracellular (CD25, CD45RO, CD45RA, CCR-7, L-Selectin [CD62L], etc.) and intracellular to markers (FOXP3), epigenetic and genetic programs and metabolic ways that defines their pathogenic value in development of allergic inflammation
The study included 90 children aged 3-11, among them 60 children with a verified diagnosis of allergen-induced bronchial asthma phenotype with mild (11.67%) and moderate severity (88.33%) clinical course of disease (44 (73.33%) bronchial asthma children combined with allergic rhinitis) and 30 healthy peers who made up the comparison group
Summary
In case of allergic diseases, imbalance in regulation of immune response to antigen is accompanied by decrease of suppressive activity of regulatory T cells, production of specific immunoglobulin antibodies IgE or implementation of delayed-type hypersensitivity reaction and allergic inflammation. The role of activated CD4+T cells of memory as the main producer of cytokines of activated T helpers of type 2 (Th2) in allergic bronchial asthma and a number of other atopic diseases has been proven. Cytokines of Th2 profile – IL-4 and IL-13 interact with resident cells of pulmonary tract, including epithelium, myofibroblasts and smooth muscle cells, as a consequence affects pathophysiological features of implementation of inflammation in bronchial asthma [3, 15]. That an increase in the number of activated T cells of memory (CD54RO/ CD25) in the lungs or peripheral blood indicated chronic inflammation in asthma. CD3+CD4+ populations (Th1, Th2, Th9, Th17, Th22, Treg and Tfh), CD3+CD8+ of memory and effector subpopulations differ on extracellular (CD25, CD45RO, CD45RA, CCR-7, L-Selectin [CD62L], etc.) and intracellular to markers (FOXP3), epigenetic and genetic programs and metabolic ways (catabolic or anabolic) that defines their pathogenic value in development of allergic inflammation
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