ArticleCurrent rheumatology reviews2025
Specific Features of Juvenile Idiopathic Arthritis Patients' Chemokine Profile: The Data of Case-Control Study Analysis.
Article in Current rheumatology reviews, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundJuvenile 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.
aimsThe study aimed to identify a list of the most informative diagnostic markers from a wide range of juvenile idiopathic arthritis patients' blood plasma chemokines.
methodsThe 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.
resultsThe 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%.
conclusionAn 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.
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