Abstract

Autoantibody formation, as a physiological mechanism of homeostatic regulation, leads to pathological processes when overexpressed. Autoantibodies are produced when the concentration of autoantigens increases, which occurs as a result of tumour necrotization and metastasizing. Autosensitization in known to develop in chronic inflammatory and tumour processes. It is of interest to clarify the significance of antiinflammatory cytokines for the formation of autoantibodies in malignant neoplasms. The purpose of this article was to identify the link between autoantibody formation and concentrations of anti-inflammatory cytokines in cancer patients. Materials and methods. Immunoassay data of 210 cancer patients of Biokor medical company (Arkhangelsk) were analysed. In the peripheral venous blood, the following were measured: antibodies against phospholipid (IgM, IgG), thyroid peroxidase (anti-TPO) and streptolysin (anti-streptolysin O), anti-double stranded DNA (anti-dsDNA) and anti-ribonucleoprotein (anti-RNP), as well as interleukins (IL) 1β, 4, 6, 10 and 13, and tumour necrosis factor (TNF-α). Results. High frequency of elevated concentrations of anti-dsDNA, antiRNP and anti-streptolysin O in the blood of cancer patients was recorded (51.72, 40.48 and 34.78 %, respectively). Most often, increased levels of anti-dsDNA were found, their mean concentrations being the highest as well. The frequency of elevated concentrations of antiphospholipid antibodies was 11.11 % for IgM and 18.42 % for IgG. Increased anti-TPO levels were observed in 14.29 % of cases. Elevated IL-10, IL-1ß and IL-4 were found in 86.90, 23.81 and 10.81 % of cased, respectively, while IL-6 and IL-13 in 5.71 and 3.85 % of cases, respectively. Mean concentrations of the cytokines under study were within the physiological limits, except for IL-10 and TNF-α, which were increased. Elevated concentrations of autoantibodies were associated with increased blood levels of TNF-α and IL-10. Thus, abnormally high blood concentrations of IL-10, which reduces cellular receptor activity, can indirectly contribute to a decrease in the activity of autoantigen disposal and clearance and prolong autosensitization.

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