» Articles » PMID: 25995033

SDF-1 and CXCR4 in Synovium Are Associated with Disease Activity and Bone and Joint Destruction in Patients with Rheumatoid Arthritis Treated with Golimumab

Overview
Journal Mod Rheumatol
Specialty Rheumatology
Date 2015 May 22
PMID 25995033
Citations 17
Authors
Affiliations
Soon will be listed here.
Abstract

Objectives: The aim of this study was to determine whether the levels of stromal cell-derived factor (SDF)-1 and its receptor C-X-C chemokine receptor 4 (CXCR4) in synovium were correlated with clinical outcome and bone and joint destruction in rheumatoid arthritis (RA) patients being treated with golimumab.

Methods: Synovial tissues were obtained from 15 golimumab-treated patients and were assessed for SDF-1 and CXCR4 using a new immunohistological scoring system (IH score). The IH score was used to assess correlations between synovial SDF-1 or CXCR4 and the disease activity score (DAS28 CRP), Rooney score, tumor necrosis factor alpha, interleukin-6 (IL-6), CD4, CD20, CD68 and the Assessment of RA by Scoring of Large-Joint Destruction and Healing in Radiographic Imaging (ARASHI) score. Receiver-operating characteristic (ROC) curves were used to predict ARASHI scores from the CXCR4 IH scores.

Results: SDF-1 strongly correlated with the DAS28 CRP and serum IL-6. CXCR4 correlated with synovial CD4 and the ARASHI score. ROC analysis of CXCR4 and ARASHI scores >10 indicated a cutoff of 12 points on the IH score for predicting joint destruction during treatment.

Conclusions: Synovial SDF-1 correlated with disease activity, and its receptor CXCR4 was related to joint destruction in RA patients treated with golimumab.

Citing Articles

CXCR4-targeted PET imaging in rheumatoid arthritis: a novel approach for monitoring disease activity and therapeutic response.

Han Y, Cao S, Liu J, Ding B, Wang S, Pan J EJNMMI Res. 2025; 15(1):10.

PMID: 39966233 PMC: 11836264. DOI: 10.1186/s13550-025-01203-z.


Low dose methotrexate impaired T cell transmigration through down-regulating CXCR4 expression in rheumatoid arthritis (RA).

Ding L, Park D, Gao B, Wu L, Li M, Abedelhakim H Arthritis Res Ther. 2024; 26(1):173.

PMID: 39350214 PMC: 11440717. DOI: 10.1186/s13075-024-03403-9.


ITIH4 in Rheumatoid Arthritis Pathogenesis: Network Pharmacology and Molecular Docking Analysis Identify CXCR4 as a Potential Receptor.

Joshi L, Chakraborty D, Kumar V, Biswas S Pathophysiology. 2024; 31(3):514-530.

PMID: 39311312 PMC: 11417925. DOI: 10.3390/pathophysiology31030038.


Revolutionizing Treatment Strategies for Autoimmune and Inflammatory Disorders: The Impact of Dipeptidyl-Peptidase 4 Inhibitors.

Rahim K, Shan M, Ul Haq I, Nawaz M, Maryam S, Alturki M J Inflamm Res. 2024; 17:1897-1917.

PMID: 38544813 PMC: 10968008. DOI: 10.2147/JIR.S442106.


The Role of CCL3 in the Pathogenesis of Rheumatoid Arthritis.

Yang Y, Li X, Song B, Wu S, Wu Y, Huang C Rheumatol Ther. 2023; 10(4):793-808.

PMID: 37227653 PMC: 10326236. DOI: 10.1007/s40744-023-00554-0.