Related Experiment Video
Updated: Jun 14, 2025

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Specific Features of Juvenile Idiopathic Arthritis Patients' Chemokine Profile: The Data of Case-Control Study
Arseniy V Rybakov1,2, Karina A Yureva1,3, Vitaliy V Khizha1
1Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences (IEFB RAS), Autoimmune and Autoinflammation Human Diseases Investigation Scientific and Practical Research Group, Saint- Petersburg, 194223, Russian Federation.
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.
Aims:
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%.
Conclusion:
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.
More Related Videos
12:36Single-cell Analysis of Immunophenotype and Cytokine Production in Peripheral Whole Blood via Mass Cytometry
Published on: June 26, 2018
08:47Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Related Concept Videos
The JAK-STAT Signaling Pathway
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...