背景:幼年特发性关节炎的发病机制涉及大量不同的免疫系统细胞,它们既是趋化因子的来源又是目标,这不仅影响他们的迁徙,也影响他们的生存,扩散,分化,所有细胞因子类型的产生,脱粒,并直接刺激或抑制血管生成。研究趋化因子对这种疾病发病机制的贡献将有可能识别新的敏感和特异性标志物,用于其诊断和随后的治疗有效性的动态监测。该研究旨在从广泛的青少年特发性关节炎患者血浆趋化因子中鉴定出信息最丰富的诊断标记。
方法:病例对照研究包括40例确诊病理患者和20例健康年龄匹配儿童。MCP-1/CCL2、MCP-3/CCL7、MIG/CXCL9、MIP-1α/CCL3、MIP-1β/CCL4、RANTES/CCL5、IFN-γ、通过酶联免疫吸附试验测定每个人血浆中的IP-10/CXCL10和MDC/CCL22。
结果:以下趋化因子被包括在最有希望的诊断标志物列表中:MCP-1,MIP-1α,MIG,RANTES,和IFN-γ。诊断为病理的患者的血浆含量比条件健康组高3至60倍(MIG)。其敏感性和特异性均超过90%。
结论:它们含量的增加导致活跃的单核细胞/巨噬细胞迁移到炎症部位,它们通过结合抑制外泌体来抑制效应T细胞活性,并通过由于关节组织破坏而接受的自身抗原呈递来激活B细胞。这使我们能够谈论在所研究的疾病慢性炎症的发展过程中Th1介导的免疫应答的优势。
BACKGROUND: Juvenile idiopathic arthritis pathogenesis involves a large number of different immune system cells, which are both sources and targets of chemokines, that affect not only their migration but also survival, proliferation, differentiation, production of all cytokine types, degranulation, and also directly stimulating or suppressing angiogenesis. Studyingthe contribution of chemokines to this disease pathogenesis will make it possible to identify new sensitive and specific markers for its diagnosis and subsequent dynamic monitoring of treatment effectiveness. The study aimed to identify a list of the most informative diagnostic markers from a wide range of juvenile idiopathic arthritis patients\' blood plasma chemokines.
METHODS: The case-control study included 40 diagnosed pathology patients and 20 healthy agematched children. The content of MCP-1/CCL2, MCP-3/CCL7, MIG/CXCL9, MIP-1α/CCL3, MIP-1β/CCL4, RANTES/CCL5, IFN-γ, IP-10/CXCL10, and MDC/CCL22 were measured by enzyme- linked immunosorbent assay in blood plasma of each person.
RESULTS: The following chemokines were included in the list of the most promising diagnostic markers: MCP-1, MIP-1α, MIG, RANTES, and IFN-γ. Their blood plasma content in patients with a diagnosed pathology was from 3 to 60 times (MIG) higher than in the conditionally healthy group. Their sensitivity and specificity exceeded 90%.
CONCLUSIONS: An increase in their content leads to active monocytes/macrophages migration to the site of inflammation, where they suppress effector T-cell activity by binding suppressor exosomes and activate B-cells by autoantigens presentation received due to joint tissue destruction. This allows us to speak about the predominance of the Th1-mediated immune response during the development of studied disease chronic inflammation.