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Monoclonal Antibody Induced Arthritis: a shorter, more synchronized alternative to the classic CIA model

Collagen-induced arthritis (CIA) in mice is widely used as an experimental model for rheumatoid arthritis. Initial symptoms of inflammation in the CIA model occur at approximately day 21-24 with the model requiring 6-8 weeks to complete. The induction of the disease is typically at 80% of the animals and varies from laboratory to laboratory and with the use of different collagen sources. The disease symptoms also appear at slightly different times in different animals, making therapeutic administration protocols more demanding technically. With the long study length, significant amounts of compounds are required to be prepared for use over the study duration. Furthermore, the lengthy study period also requires increased number of measurements and scoring periods, increasing the cost of the study further. These points illustrate some of the key issues in running a typical CIA model. The monoclonal antibody induced arthritis model (mAb-induced RA, AIA or CAIA) is ideal for rapidly screening and evaluating anti-inflammatory therapeutic agents providing more information in a shorter amount of time. The flexibility of the system means it is applicable to the wide range of DBA, Balb/c, C57bl/6 as well transgenic strain bred on the C57Bl background. It is also relevant for studying inflammatory mediators such as cytokines, chemokines, matrix metalloproteinases and other factors such as the role of bacterial flora and their by-products in triggering and exacerbating arthritis.

The antibody cocktail of collagen type II antibodies selected for their epitope specificity can induce rapid arthritis with 100% synchronicity. The ArthritoMab™ Antibody Cocktail (Cat. no. CIA-MAB) consists of four monoclonal antibodies to CII that bind to the well-defined epitopes C1, J1, D3, and U1. These epitopes are spread across the entire CII region, are found in mice immunized with CII and developing arthritis and encourage better immune complex formation on the cartilage surface or in the synovium. These complexes can then activate, complement, and induce inflammation by both the classical and alternative pathways. Monocytes in the joint are also activated by these complexes via Fc receptors releasing pro-inflammatory cytokines, (i.e., TNF-α and IL-1β), which recruit neutrophils and macrophages.

To read more about the Collagen Antibody-induced Arthritis Model (CAIA) or the antibodies in the ArthritoMab™ Antibody Cocktail, download a complimentary whitepaper. 

ArthritoMab™ Antibody Cocktail50mgCIA-MAB-50Balb/c, DBA/1, R10.RIII
ArthritoMab™ Antibody Cocktail for C57bl/650mgCIA-MAB-2CC57bl/6

Selection of recent Publications

Cambré, Isabelle, et al. "Running promotes chronicity of arthritis by local modulation of complement activators and impairing T regulatory feedback loops. Annals of the rheumatic diseases 78.6 (2019): 787 - 795.

Alshammari, A., & Amar, S. (2019). Proposal for a novel murine model of human periodontitis using Porphyromonas gingivalis and type II collagen antibody injections. The Saudi Dental Journal.

Hand, L. E., Dickson, S. H., Freemont, A. J., Ray, D. W., & Gibbs, J. E. (2019). The circadian regulator Bmal1 in joint mesenchymal cells regulates both joint development and inflammatory arthritis. Arthritis research & therapy21(1), 5.

Borbély, É., Kiss, T., Szabadfi, K., Pintér, E., Szolcsányi, J., Helyes, Z., & Botz, B. (2018). Complex Role of Capsaicin-Sensitive Afferents in the Collagen Antibody-Induced Autoimmune Arthritis of the Mouse. Scientific reports8(1), 15916.

Huck, O., You, J., Han, X., Cai, B., Panek, J., & Amar, S. (2018). Reduction of Articular and Systemic Inflammation by Kava-241 in Porphyromonas gingivalis-induced Arthritis Murine Model. Infection and immunity, IAI-00356.