Loading…

A study of the association between Galectin-9 gene (LGALS9) polymorphisms and rheumatoid arthritis in Egyptian patients

Background Rheumatoid arthritis (RA) is an incessant synovial inflammation of an autoimmune origin, destroying articular cartilages and bones. Galectins are an evolutionarily conserved family of immune-modulatory animal lectins detected in a number of immune cells like T cells, fibroblasts and macro...

Full description

Saved in:
Bibliographic Details
Published in:Egyptian Rheumatology and Rehabilitation 2023-07, Vol.50 (1), p.30-10, Article 30
Main Authors: Ameen, Seham Gouda, Zidan, Magda Abd el-Aziz, Amer, Arwa S., Elshahat, Nessma Fathy, Elhalim, Walid Abd Ellatif Abd
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Background Rheumatoid arthritis (RA) is an incessant synovial inflammation of an autoimmune origin, destroying articular cartilages and bones. Galectins are an evolutionarily conserved family of immune-modulatory animal lectins detected in a number of immune cells like T cells, fibroblasts and macrophages. Galectin 9 (Gal-9) has been the subject of many studies for being linked to regulation of both innate and adaptive immune reactions. The objective of the study was to evaluate the link between the Galectin-9 gene (LGALS9) polymorphisms and the susceptibility of RA in Egyptian patients, as well as, detection of the serum level of Gal-9 in RA and its association with LGALS9 polymorphisms, the activity of RA and radiological damage. Methods A study of 85 participants; group (I): 60 RA cases and group (II): 25 apparently healthy subjects. RA Disease activity index (DAS-28) and Larsen index score were assessed. LGALS9 gene and serum Gal-9 were investigated. Results rs4239242 TT genotype and T allele occurred more frequently in RA cases than controls with a significant difference ( P  = 0.006; P  
ISSN:2090-3235
1110-161X
2090-3235
DOI:10.1186/s43166-023-00198-6