CCR2-Deficient Mice and Autoimmune Arthritis
Author Information
Author(s): Rampersad Rishi R., Tarrant Teresa K., Vallanat Christopher T., Quintero-Matthews Tatiana, Weeks Michael F., Esserman Denise A., Clark Jennifer, Di Padova Franco, Patel Dhavalkumar D., Fong Alan M., Liu Peng
Primary Institution: University of North Carolina at Chapel Hill
Hypothesis
Skewing of Th17 cells and Th17-cell responses may account for the exacerbated arthritis in CCR2−/− mice.
Conclusion
CCR2 deficiency leads to enhanced Th17-cell responses and increased susceptibility to autoimmune arthritis.
Supporting Evidence
- Th17 cells were expanded approximately 3-fold in CCR2−/− mice compared to WT controls.
- Levels of IL-17A and other cytokines were significantly elevated in CCR2−/− mice.
- Treatment with anti-IL-17A antibody reduced disease severity in CCR2−/− mice.
Takeaway
Mice without a certain protein (CCR2) get much worse arthritis because their immune system makes too many Th17 cells, which cause inflammation.
Methodology
The study involved inducing collagen-induced arthritis in CCR2−/− mice and analyzing Th17 cell responses, cytokine levels, and disease severity.
Potential Biases
Potential bias due to the involvement of authors from a pharmaceutical company.
Limitations
The study primarily focuses on a mouse model, which may not fully replicate human autoimmune conditions.
Participant Demographics
8–10 week-old male mice were used in the experiments.
Statistical Information
P-Value
0.017
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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