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Updated: Jul 19, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
sE-Selectin expression and A561C polymorphism in relation to rheumatoid arthritis clinical activity
Rosa Elena Navarro-Hernández1, Edith Oregón-Romero, Héctor Rangel-Villalobos
1Doctorado en Ciencias Biomédicas, Orientación en Inmunología-Laboratorio de Inmunología, Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético, Centro Universitario de Ciencias de la Salud, Jalisco, Mexico.
Objective:
To investigate the relationship of A561C polymorphism and sE-selectin levels with rheumatoid arthritis (RA) clinical activity.
Methods:
In a case-control study, we compared 60 patients with RA and 60 healthy subjects. Patients fulfilled the 1987 American College of Rheumatology criteria. Soluble E-selectin levels were measured from serum samples using the ELISA kit. We investigated E-selectin A561C polymorphism by the restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) technique. The disease activity was recorded with Spanish Health Assessment Questionnaire Disability Index (HAQ-DI), Spanish Arthritis Impact Measurement Scales (AIMS), and Disease Activity Score (DAS28) scores. A p value < 0.05 was considered significant.
Results:
Patients with RA showed higher sE-selectin levels than controls (mean 91.7 vs 39 ng/ml; p = 0.002). A positive correlation between sE-selectin and rheumatoid factor (RF), erythrocyte sedimentation rate (ESR), Spanish HAQ-DI, and DAS28 scores was found. The E-selectin polymorphism analysis showed diminished frequency in RA of heterozygous A/C genotype and increased frequency of homozygous wild-type A/A genotype (p = 0.043, OR 1.45; 95% CI 1.125-16.167) versus A/C and A/A genotype in healthy subjects. No significant association between A561C polymorphism and clinical activity was present.
Conclusion:
The sE-selectin, RF, and ESR, in addition to clinical indices, were associated with clinical activity in RA. We highlighted the presence of A/A genotype A561C polymorphism in our patients with RA.
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