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B cell-deficient mice do not develop type II collagen-induced arthritis (CIA)
L Svensson1, J Jirholt, R Holmdahl
1Section for Medical Inflammation Research, CMB, Lund University, Sweden.
Clinical and Experimental Immunology
|April 7, 1998
Summary
B cells are crucial for developing collagen-induced arthritis (CIA), a rheumatoid arthritis model. Mice lacking B cells showed no CIA development, indicating their essential role in this autoimmune disease.
Area of Science:
- Immunology
- Autoimmunity
- Rheumatoid Arthritis Research
Background:
- Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation.
- Collagen-induced arthritis (CIA) is a widely used mouse model to study RA pathogenesis.
- The specific role of B cells in CIA development requires further elucidation.
Purpose of the Study:
- To investigate the essential role of B cells in the development of collagen-induced arthritis (CIA).
- To determine if B cell absence impacts the T cell response in CIA models.
Main Methods:
- Utilized mice genetically engineered to lack B cells by deleting the IgM heavy chain gene (muMT).
- Backcrossed muMT mice into CIA-susceptible B10.Q and B10.RIII strains.
- Induced CIA using rat type II collagen (CII) in B10.Q and bovine CII in B10.RIII mice.
- Assessed CIA susceptibility and anti-CII T cell responses in muMT versus wild-type mice.
Main Results:
- Homozygous deletion of the IgM gene resulted in a complete absence of B cells and significantly reduced immunoglobulin levels.
- The absence of B cells completely abrogated the development of CIA in both mouse strains.
- No significant difference was observed in the anti-CII T cell response between B cell-deficient (muMT) and wild-type mice.
Conclusions:
- B cells play a critical and indispensable role in the development of collagen-induced arthritis.
- The pathogenic mechanism of CIA development in this model is dependent on B cells, independent of the T cell response to collagen.