@article{ACERJMB202551261,
    title = {Impact of CD39 and CD73 Expression in Rheumatoid Arthritis Patients Mohammed},
    journal = {ACE Research Journal of Microbiology and Biotechnology},
    volume = {5},
    number = {1},
    pages = {1-4},
    year = {2025},
    issn = {2520-3975},
    doi = {10.36478/acerjmb.2025.1.4},
    url = {https://theacepublications.com/article-detail.php?art=261-ACE-RJMB},
    author = {Anwar and},
    keywords = {Rheumatoid arthritis, CD39, interleukin‐6, cytokines, purinergic signaling, gene expression},
    abstract = {Rheumatoid arthritis (RA) is a chronic autoimmune disorder
characterized by persistent synovial inflammation, progressive joint
damage and systemic manifestations. The condition arises from a
complex interplay of genetic predisposition, environmental triggers and
immune dysregulation. A hallmark of RA is the disruption of cytokine
signaling, which promotes continuous inflammation and tissue
destruction. Recent focus has shifted toward understanding the role of
purinergic signaling, particularly through ectonucleotidases like CD39,
which regulate extracellular ATP and immune cell responses. This study
aimed to assess the expression levels of CD39 in peripheral blood
mononuclear cells (PBMCs) of RA patients and evaluate its relationship
with interleukin‐6 (IL‐6) levels. The goal was to explore the potential
involvement of CD39 in the immunopathogenesis of RA. A case‐control
study was conducted involving 100 participants, divided equally into RA
patients and healthy controls. CD39 gene expression in PBMCs was
quantified using qRT‐PCR, while serum IL‐6 levels were measured using
ELISA. Demographic and clinical data were collected, and molecular
analyses were carried out on extracted RNA samples. The findings
showed a significant downregulation of CD39 expression in RA patients
compared to healthy individuals (p<0.0019), suggesting impaired ATP
hydrolysis and a possible role in sustaining inflammation. Concurrently,
IL‐6 levels were markedly elevated in RA patients, with a significant
correlation between IL‐6 and disease markers such as RF and ESR. The
data also revealed a negative correlation between CD39 and CD73
expression levels in patients. The results support the hypothesis that
disrupted purinergic signaling, marked by reduced CD39 expression,
contributes to RA pathogenesis. Elevated IL‐6 further emphasizes the
inflammatory state. CD39 and IL‐6 could serve as valuable biomarkers
for understanding disease mechanisms and tailoring personalized
therapies.}
    }