Cellular reactions of CD3+ CD4+ CD45RO+ T-lymphocytes on dexamethason in in normal patients and in patients with with rheumatoid arthritis in vitro

Autor: L. S. Litvinova, N. M. Todosenko, O. G. Khaziakhmatova, I. P. Malinina, K. A. Yurova
Jazyk: English<br />Russian
Rok vydání: 2018
Předmět:
Zdroj: Бюллетень сибирской медицины, Vol 16, Iss 4, Pp 207-219 (2018)
Druh dokumentu: article
ISSN: 1682-0363
1819-3684
DOI: 10.20538/1682-0363-2017-4-207-219
Popis: The aim of the study was to analyze the influence of glucocorticoid (GC) dexamethasone (Dex) on changes in CD4+ T-cells expressing the surface molecule of activation (CD25, CD71, HLA-DR and CD95) and their ability to produce proinflammatory mediators in cultures of TCR-stimulated CD3+CD45RO+ T-lymphocytes obtained from healthy donors and patients with rheumatoid arthritis in vitro.Materials and methods. The study included 50 patients and 20 healthy donors. T-cell cultures (CD3+ CD45RO+) were obtained from mononuclear leukocytes of immunomagnetic separation (MACS® technology). As an activator of T-lymphocytes, antibiotic particles with biotinylated antibodies against CD2+, CD3+, CD28+, which simulate the process of costimulation of T cells by antigen-presenting cells, were used. The following concentrations of dexamethasone (2, 8, 16, 32, 64 mg) were used in the experiment. The change in the immunophenotype of T-lymphocytes was analyzed by flow cytofluoometry. The secretion of CD3+CD45RO+ T-cells of proinflammatory cytokines IL-2, IFNγ, TNFα, IL-17 and IL-21 was evaluated by enzyme-linked immunosorbent assay.Results. The general suppressor effect of Dex on CD3+CD45RO+ T-cell cultures mediated by a decrease in the number of CD4 + T cells expressing activation molecules (CD25) and proliferation (CD71), as well as inhibition of the production of inflammatory mediators: IFNγ, IL-2 and TNFα. It is shown that against the background of TCR activation Dex increases the number of CD4+CD95+HLA-DR+ cells in CD3+CD45RO+ cultures obtained from RA patients and does not change their content in the control. The correlations between the number of proinflammatory factors (IL-17, IL-21 and TNFα) in CD4+CD45RO+CD95+HLA-DR+ T cells in supernatants of cell cultures in RA patients indicate the presence of a pro-inflammatory potential of this population of T cells. We assume that the resistance of CD4+CD45RO+CD95+HLA-DR+ T cells in RA patients to the suppressor effect of GC generally leads to the preservation and enhancement of the functionality of autoreactive cells in the pathogenesis of RA.
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