ArticleEuropean journal of immunology2021
CCL25 and CCR9 is a unique pathway that potentiates pannus formation by remodeling RA macrophages into mature osteoclasts.
Article in European journal of immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Identification of new overlapping and disease-specific genetic risk factors for rheumatoid arthritis and radiographic axial spondyloarthritis: a meta-analysis of three large European populations and functional characterization.Frontiers in immunology · 2026Pooled it
- Review
- Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Human peripheral osteoclast-precursor-development patterns reveal the significance of RPS17-dependent ribosome synthesis to Ankylosing Spondylitis lesions.Bone research · 2025Article
- The causal relationship between inflammatory cytokines and lung cancer: a two-sample bidirectional mendelian randomization study.Discover oncology · 2025Article
- Deciphering the role of ERK and PI3K/Akt as crosstalk pathways between fibroblast-like synoviocytes and osteoclasts; novel therapeutic approach for rheumatoid arthritis.Molecular biology reports · 2025Review
- Lycium barbarum polysaccharide corrects CCR9Clinical rheumatology · 2025Article
- MAPK/ERK signaling pathway in rheumatoid arthritis: mechanisms and therapeutic potential.PeerJ · 2025Review
- Multi-omic Biomarkers Distinguish Rheumatoid Arthritis in Discordant Monozygotic Twins.medRxiv : the preprint server for health sciences · 2024Article
- Detecting global and local hierarchical structures in cell-cell communication using CrossChat.Nature communications · 2024Article
- Article
- Inhibition of Cdc37 Ameliorates Arthritis in Collagen-Induced Arthritis Rats by Inhibiting Synoviocyte Proliferation and Migration Through the ERK Pathway.Inflammation · 2023Article
- ZIM3 activation of CCL25 expression in pulmonary metastatic nodules of osteosarcoma recruits M2 macrophages to promote metastatic growth.Cancer immunology, immunotherapy : CII · 2023Article
- Immunomodulatory Microparticles Epigenetically Modulate T Cells and Systemically Ameliorate Autoimmune Arthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Chemokines and chemokine receptors as promising targets in rheumatoid arthritis.Frontiers in immunology · 2023Review
- G-Protein-Coupled Receptors in Rheumatoid Arthritis: Recent Insights into Mechanisms and Functional Roles.Frontiers in immunology · 2022Review
- Three Classes of Antioxidant Defense Systems and the Development of Postmenopausal Osteoporosis.Frontiers in physiology · 2022Review
- The Macrophage-Osteoclast Axis in Osteoimmunity and Osteo-Related Diseases.Frontiers in immunology · 2021Review
- Macrophages: The Good, the Bad, and the Gluttony.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
This study elucidates the mechanism of CCL25 and CCR9 in rheumatoid arthritis (RA). RA synovial fluid (SF) expresses elevated levels of CCL25 compared to OA SF and plasma from RA and normal. CCL25 was released into RA SF by fibroblasts (FLS) and macrophages (MΦs) stimulated with IL-1β and IL-6. CCR9 is also presented on IL-1β and IL-6 activated RA FLS and differentiated MΦs. Conversely, in RA PBMCs neither CCL25 nor CCR9 are impacted by 3-month longitudinal TNF inhibitor therapy. CCL25 amplifies RA FLS and monocyte infiltration via p38 and ERK phosphorylation. CCL25-stimulated RA FLS secrete potentiated levels of IL-8 which is disrupted by p38 and ERK inhibitors. CCL25 polarizes RA monocytes into nontraditional M1 MΦs that produce IL-8 and CCL2. Activation of p38 and ERK cascades are also responsible for the CCL25-induced M1 MΦ development. Unexpectedly, CCL25 was unable to polarize RA PBMCs into effector Th1/Th17 cells. Consistently, lymphokine like RANKL was uninvolved in CCL25-induced osteoclastogenesis; however, this manifestation was regulated by osteoclastic factors such as RANK, cathepsin K (CTSK), and TNF-α. In short, we reveal that CCL25/CCR9 manipulates RA FLS and MΦ migration and inflammatory phenotype in addition to osteoclast formation via p38 and ERK activation.
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Registered trials
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