The relationship of FoxP3+ T regulatory cells to disease activity and antibody levels in early rheumatoid arthritis

Автор: Avdeeva A.S., Rubtsov Yu.P., Dyikanov D.T., Popkova T.V., Nasonov E.L.

Журнал: Научно-практическая ревматология @journal-rsp

Рубрика: Оригинальные исследования

Статья в выпуске: 3 т.55, 2017 года.

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Objective: to analyze the relationship of the count of FoxP3+ T regulatory cells (Tregs) to the clinical and laboratory parameters of disease activity and the levels of antibodies in a group of patients with early rheumatoid arthritis (RA). Subjects and methods. The investigation enrolled 45 patients with early RA (2010 ACR/EULAR criteria) who had not previously received treatment with methotrexate, including 39 women; median age was 52.0 [32.5; 57.5] years; disease duration, 5 [4; 6] months, DAS28 5.01 [4.18; 5.8]; 71.1% of the patients were rheumatoid factor (RF) positive and 88.9% were anti-cyclic citrullinated peptide positive. The relative and absolute counts of Treg (FoxP3+CD25+; CD152+surface; CD152+intracellular; FoxP3+CD127-; CD25+CD127-; FoxP3+ICOS+; FoxP3+CD154+; FoxP3+CD274+) were measured by immunofluorescence staining and multicolor flow cytometry. A control group consisted of 20 healthy donors who were matched for sex and age with the examined patients. Results and discussion. DАS28 was high, moderate, and low in 22 (48.9%), 20 (44.4%), and 3 (6.7%) patients, respectively. As compared with the healthy donors, the patients with early RA were observed to have lower values in the percentage of FoxP3+CD25+ cells, in the percentage and absolute count of FoxP3+ICOS+ cells, in the percentage and absolute count of FoxP3+CD154+ and FoxP3+ CD274+ T cells; preg were decreased in early RA, which is associated with higher disease activity, the systemic manifestations of the disease and which is also accompanied by antibody hyperproduction.

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Early rheumatoid arthritis, disease activity, autoantibodies, t regulatory lymphocytes

Короткий адрес: https://sciup.org/14945818

IDR: 14945818   |   DOI: 10.14412/1995-4484-2017-245-251

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