Toll-like receptor homolog RP105 modulates the antigen-presenting cell function and regulates the development of collagen-induced arthritis
2008

RP105's Role in Collagen-Induced Arthritis

Sample size: 53 publication 10 minutes Evidence: moderate

Author Information

Author(s): Tada Yoshifumi, Koarada Syuichi, Morito Fumitaka, Mitamura Mio, Inoue Hisako, Suematsu Rie, Ohta Akihide, Miyake Kensuke, Nagasawa Kohei

Primary Institution: Saga Medical School

Hypothesis

RP105 modulates the antigen-presenting cell function and regulates the development of collagen-induced arthritis.

Conclusion

RP105 regulates the antigen-presenting cell function and Treg development, which suppresses the development of collagen-induced arthritis.

Supporting Evidence

  • RP105-deficient mice showed accelerated onset of arthritis and increased severity.
  • Interferon-gamma and tumor necrosis factor-alpha production by spleen cells from RP105-deficient mice was increased compared to wild-type mice.
  • RP105-deficient mice had more severe arthritis induced by collagen with incomplete Freund's adjuvant.

Takeaway

This study found that mice without RP105 got arthritis faster and more severely, showing that RP105 helps control the immune response.

Methodology

Collagen-induced arthritis was induced in RP105-deficient DBA/1 mice, and the incidence and severity of arthritis were analyzed along with cytokine production.

Limitations

The study did not determine the precise role of TLRs due to potential contamination of LPS with TLR2 ligands.

Participant Demographics

Mice were 12 to 16 weeks old, with both male and female subjects used.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1186/ar2529

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication