免疫炎症性风湿病（IRD）的发病机制基于慢性炎症，其关键机制之一可能是巨噬细胞的异常激活，导致免疫系统进一步破坏。本研究的目的是评估促炎性激活IRD 患者循环单核细胞的数量。该研究涉及 149 名参与者（53 名类风湿性关节炎 (RA) 患者、45 名系统性红斑狼疮 (SLE) 患者、34 名系统性硬皮病 (SSc) 患者和 17 名无 IRD 的参与者）30至65岁。在通过免疫磁性分离从血液中获得的单核细胞的原代培养物中研究了基础和脂多糖（LPS）刺激的单核细胞分泌。通过ELISA对培养液中的细胞因子肿瘤坏死因子α（TNF-α）、白细胞介素1β（IL-1β）以及趋化因子单核细胞趋化蛋白-1（MCP-1）进行定量评估。单核细胞的促炎激活被计算为LPS刺激的分泌物与基础分泌物的比率。结果显示，所有研究的细胞因子的基础分泌物在所有IRD患者组中均显着增加，除了IL-1β的分泌物在IRDs患者中显着增加。 SLE 组与对照组相比。与对照组相比，IRD 患者 LPS 刺激的 TNF-α 分泌增加，MCP-1 减少； LPS 刺激的 IL-1β 分泌仅在 SSc 组中与对照组有显着差异。在 RA 组中，与对照组相比，所有细胞因子的单核细胞活化均减少；在 SLE 组中，针对 TNF-α 和 MCP-1；在 SSc 组中，对于 MCP-1.. IRD 患者中单核细胞促炎性激活的减少是由于细胞因子基础分泌水平高，这可能导致这些疾病中充分免疫反应的破坏，并且是慢性炎症发病机制中的重要环节。© 2024. Pleiades Publishing, Ltd.

The pathogenesis of immunoinflammatory rheumatic diseases (IRDs) is based on chronic inflammation, one of the key mechanisms of which may be abnormal activation of macrophages, leading to further disruption of the immune system.. The objective of this study was to evaluate the proinflammatory activation of circulating monocytes in patients with IRDs.. The study involved 149 participants (53 patients with rheumatoid arthritis (RA), 45 patients with systemic lupus erythematosus (SLE), 34 patients with systemic scleroderma (SSc), and 17 participants without IRDs) 30 to 65 years old. Basal and lipopolysaccharide (LPS)-stimulated secretion of monocytes was studied in a primary culture of monocytes obtained from blood by immunomagnetic separation. Quantitative assessment of the cytokines tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), as well as the chemokine monocyte chemoattractant protein-1 (MCP-1) was carried out in the culture fluid by ELISA. Proinflammatory activation of monocytes was calculated as the ratio of LPS-stimulated and basal secretions.. It was shown that the basal secretion of all studied cytokines was significantly increased in all groups of patients with IRDs, except for the secretion of IL-1β in the SLE group, compared to the control. LPS-stimulated secretion of TNF-α was increased and MCP-1 was decreased in patients with IRDs compared to the control group; LPS-stimulated IL-1β secretion only in the SSc group significantly differed from the control group. In the RA group, monocyte activation was reduced for all cytokines compared to the control; in the SLE group, for TNF-α and MCP-1; in the SSc group, for MCP-1.. The decrease in proinflammatory activation of monocytes in patients with IRDs is due to a high level of basal secretion of cytokines, which can lead to disruption of the adequate immune response in these diseases and is an important link in the pathogenesis of chronic inflammation.© 2024. Pleiades Publishing, Ltd.