Open AccessINDICES OF CELL-MEDIATED IMMUNITY IN RHEUMATOID ARTHRITIS: THE ROLE OF CYTOMEGALOVIRUS INFECTION
Author(s) -
А. В. Чуров,
Anastasia Novitskaya,
С. Н. Коломейчук,
Е. К. Олейник
Publication year - 2019
Publication title -
kliničeskaâ laboratornaâ diagnostika
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.12
H-Index - 10
eISSN - 2412-1320
pISSN - 0869-2084
DOI - 10.18821/0869-2084-2019-64-2-98-103
Subject(s) - immunology , foxp3 , il 2 receptor , immune system , antibody , rheumatoid arthritis , immunity , cd8 , cd3 , pathogenesis , biology , t cell , medicine
The pathogenesis of rheumatoid arthritis (RA) is driven by a combined action of genetic and environmental factors, which can upset the balance between the effector and regulatory components of the immune system. An important actor in maintaining such balance is T cells, especially regulatory T lymphocytes (Treg), but the mechanisms behind the functioning of T cell subpopulations and the roles of individual etiological factors in RA have not been fully elucidated. This study aimed to investigate the indices of cell-mediated immunity, especially T- and Treg cells, in RA patients depending on the disease activity and presence of cytomegalovirus (CMV) infection. The expression of membrane and intracellular molecular markers of lymphocytes was estimated by multicolor flow cytometry. The content of antibodies to CMV in blood plasma was measured by enzyme immunoassays. Patients with RA had reliably reduced numbers of cells with the phenotypes CD4+FOXP3+, CD4+CD25+FOXP3+ correlating with the stage of RA activity. RA patients with CMV infection showed a reduction in the number of regulatory T cells (Treg), CD3+ T lymphocytes, CD3+CD8+ cells in peripheral blood. At the same time, RA involved a rise in the level of B cells and CD4+CD25+ Т cells. The level of antibodies to CMV was observed to grow in line with RA activity. Thus, the data obtained suggest that the presence of CMV infection can significantly influence the state of individual lymphocyte subpopulations during RA development.