K/BxN mice spontaneously develop a severe, chronic, progressive inflammatory arthritis at about 27 days of age. They develop auto-antibodies recognizing glucose-6-phosphate isomerase. Serum from these animals when transferred to recipient animals induce arthritis. The mechanism of action involves complement, mast cells, neutrophils and inflammatory mediators. This model is widely used for studying the humoral response in rheumatoid arthritis (RA) and models the effector phase of the disease.
The collagen antibody induced arthritis model (CAIA, also called anti-collagen induced arthritis) uses of cocktail of 4 collagen type II (CII) antibodies to induce arthritis. The antibodies bind to well-defined epitopes associated with arthritis. In this way, the CAIA model and the K/BxN model are very similar, relying on passive transfer of antibodies to induce arthritis. The severity, mechanisms of action and length of disease are similar giving similar disease scores and histology.
There are however, significant differences, which make running the CAIA model an advantage over the K/BxN:
- Epitope location: GP6i is ubiquitously expressed while CII has a restricted distribution and is concentrated in the joints ensuring antibody is directed to the site of interest.
- K/BxN sera is an undefined polyclonal mixture that can vary batch to batch. The CAIA model uses the ArthritoMab™ Antibody cocktail which is a defined and standardized mixture so there is no batch variation.
- With CAIA, arthritis is induced by clinically relevant anti-collagen antibodies.
- There is no need to maintain expensive colonies.
- Easy and constant availability of induction material.
- No waiting for animals to develop arthritis before harvesting sera.
- No concerns about colonies going down through sickness or breeding issues.