ArticleReumatologia2016
Different expression of chemokines in rheumatoid arthritis and osteoarthritis bone marrow.
Article in Reumatologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- New Paradigm for Rheumatoid Arthritis Treatment: A Review of 'Crosstalk' Mechanism of Multi-Targeted Intervention on Cytokine/Chemokine Networks by Chinese Medicine.Chinese journal of integrative medicine · 2026Review
- The intersection of GRK2 and PGE2 in rheumatoid arthritis: a comprehensive update on pathophysiology and treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Paroxetine alleviates dendritic cell and T lymphocyte activation via GRK2-mediated PI3K-AKT signaling in rheumatoid arthritis.Chinese medical journal · 2025Article
- Cytokines and chemokines multiplex analysis in patients with low disease activity rheumatoid arthritis.Rheumatology international · 2022Article
- Antibodies to Citrullinated Proteins (ACPA) Associate with Markers of Osteoclast Activation and Bone Destruction in the Bone Marrow of Patients with Rheumatoid Arthritis.Journal of clinical medicine · 2021Article
- Identification of genes and pathways in the synovia of women with osteoarthritis by bioinformatics analysis.Molecular medicine reports · 2018Article
- Rheumatoid arthritis bone marrow environment supports Th17 response.Arthritis research & therapy · 2017Article
- The therapeutic potential of targeting chemokine signalling in the treatment of chronic pain.Journal of neurochemistry · 2017Review
- Paroxetine alleviates T lymphocyte activation and infiltration to joints of collagen-induced arthritis.Scientific reports · 2017Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesRheumatoid arthritis (RA) is a chronic inflammatory disease leading to joint destruction. In addition to involvement of the joints, there is growing evidence that inflammatory/autoimmune processes take place in bone marrow, beginning the disease onset. Activated T and B cells accumulate in bone marrow, where also effective antigen presentation takes place. An increased number of activated T cells was observed in RA in comparison to osteoarthritis (OA) bone marrow. In the present study we analyzed the levels of chemokines that may be responsible for accumulation/retention of T-cells in the bone marrow of RA and OA patients. MATERIAL AND
methodsBone marrow samples were obtained from RA and OA patients during total hip replacement surgery, and bone marrow plasma was obtained by gradient centrifugation. Levels of the chemokines CX3CL1, CCL5, CCL2, CXCL12 and CXCL1 were measured in bone marrow plasma by specific ELISAs. Comparison between the groups of patients and statistical significance were analyzed by the two-tailed Mann-Whitney U test.
resultsIncreased levels of CX3CL1 (818 ±431 pg/ml vs. 502 ±131 pg/ml, p < 0.0007) and CCL5 (5967 ±1680 pg/ml vs. 4878 ±2360 pg/ml, p < 0.05) respectively in bone marrow plasma from RA in comparison with OA patients were observed. In contrast, similar levels of CCL2, CXCL12 and CXCL1 in RA and OA bone marrow suggest that these cytokines do not play a significant role in the observed T cell accumulation in RA bone marrow.
conclusionsCX3CL1 and CCL5 overproduced in RA bone marrow may contribute to the accumulation of T cells observed in RA bone marrow.
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