ArticleArthritis research & therapy2024
Low dose methotrexate impaired T cell transmigration through down-regulating CXCR4 expression in rheumatoid arthritis (RA).
Article in Arthritis research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Therapeutic effects of ginkgetin on rheumatoid arthritis: evidence from network pharmacology and experimental validation.Clinical rheumatology · 2026Article
- Emerging mechanistic trends and clinical efficacy for methotrexate: Applications to inflammatory bowel disease.Pharmacological reviews · 2026Review
- Immunometabolic and brain structural alterations mediate increased risk of brain diseases in rheumatoid arthritis patients.Translational psychiatry · 2025Article
- Integrating clinical features, inflammatory markers, and immune profiles: a Yunke-based nomogram model for rheumatoid arthritis prognosis.Frontiers in medicine · 2025Article
- Autoimmune disease-associated lymphomas: research progress and review.Frontiers in immunology · 2025Review
- The story of clobenpropit and CXCR4: can be an effective drug in cancer and autoimmune diseases?Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundCXC chemokine CXCL12 is involved in the pathological development of rheumatoid arthritis (RA) through abnormal migration of peripheral immune cells in the joint. Although low dose methotrexate (MTX) is clinically used to treat RA patients, CXCL12 signaling responses to MTX-mediated treatments is still not well understood.
methodsIn this study, we examined the expression of CXCR4 (cognatic receptor for CXCL12) in peripheral T cells from RA patients and arthritis mice models received from low dose MTX therapies. The effects of low dose MTX on CXCR4 were further determined via both in vitro CD3
resultsOur clinical data shows that low dose MTX treatment was clinically associated with down-regulated expression of chemokine receptor CXCR4 on patient peripheral T cells. In vitro, low dose MTX significantly decreased cell transmigration through down-regulated CXCR4's expression in CD3
conclusionOur findings suggest that the effect of low dose MTX treatment could serve to eliminate inflammation in RA patients through impairment of immune cell transmigration mediated by CXCR4.
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