How TNFα and Adalimumab Affect CD36 in Human Monocytes
Author Information
Author(s): Boyer Jean Frédéric, Balard Patricia, Authier Hélène, Faucon Bruno, Bernad José, Mazières Bernard, Davignon Jean-Luc, Cantagrel Alain, Pipy Bernard, Constantin Arnaud
Primary Institution: Université Paul Sabatier
Hypothesis
CD36 expression in human monocytes is regulated by TNFα and by adalimumab.
Conclusion
TNFα inhibits CD36 expression while adalimumab increases it, suggesting a potential therapeutic role in cardiovascular risk management for rheumatoid arthritis patients.
Supporting Evidence
- TNFα inhibits both CD36 membrane expression and mRNA expression.
- Adalimumab increases both CD36 membrane expression and mRNA expression.
- The induction of CD36 expression by adalimumab involves redox signaling via NADPH oxidase activation.
Takeaway
This study shows that a protein called TNFα stops a receptor called CD36 from working, but a medicine called adalimumab helps CD36 work better.
Methodology
Human monocytes were isolated from healthy donors and treated with TNFα and adalimumab to assess CD36 expression using flow cytometry and RT-PCR.
Limitations
Further studies are needed to explore the clinical implications of these findings.
Participant Demographics
Healthy donors were used for monocyte isolation.
Statistical Information
P-Value
p = 0.0004
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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