- Overview
- Data/Specifications
- Literature/Support
- How To Use
- Related Products
Overview
Collagen-induced arthritis (CIA) in mice is widely used as an experimental model for rheumatoid arthritis (RA) in humans. CIA is mediated by autoantibodies, which bind to a particular region of type II collagen (CII). The ability to induce arthritis using this arthritogenic antibody cocktail provides an efficient protocol for the induction of antibody-mediated arthritis that can be used as a shorter, more synchronized alternative to the CIA model.
Benefits of the CAIA model
- Length of study: Arthritis develops in mice typically within 24-48 hr allowing the completion of a study within 2 weeks reducing the number of assessments and scoring periods.
- Reduced group size: Rate of incidence is nearly 100% depending on the strain allowing for smaller group sizes.
- Synchronization: onset of disease is synchronized between animals simplifying treatment schedules.
- Steady & Controlled Disease Progression: evaluate various regimes with a steady disease progression. No rapid & severe disease spikes to contend with.
- Susceptibility: Induce arthritis in transgenic strains with as little as 2 mg of Antibody.
Comparison
| ArthritoMab™ | Competitor | |
Epitopes Recognized | CB11, CB10, CB8 | CB11 only |
| Disease Progression | Steady & Controlled | Rapid & Severe |
| Paw involvement | Consistent & Predominantely rear | Variable & unpredictable |
| Amount required for C57Bl/6 | 2 mg (25 animals per vial) | 5 mg (8 animals per vial) |
Abreviations:
- Anti-Collagen Induced arthritis (ACIA)
- Monoclonal Antibody induced arthritis (mAb-RA)
- Collagen Antibody Induced Arthritis (CAIA)
Data/Specifications
Epitope specificity
The classic CIA model is mediated by autoantibodies which bind totypeII collagen and complement. In mice as well as human RA patients,theantibody response that best correlates with disease is directedagainstthe C1, J1 and U1 epitopes. The ArthritoMab™ arthritogeniccocktail of 4 monoclonal antibodies binds to these well-defined epitopesC11b, J1, D3 and U1, which are spread over the entire CII (CB8, CB10and CB11 fragments). This possibly encourages better immune complexformation on the cartilage surface for the initiation of arthritis andproduces consistent and predictable disease in all 4 paws (withpredominance for the rear). Competitor products only recognize CB11,which produces variable disease that can contribute to unpredictableinvolvement in the paws (sometimes more front paw involvment and othertimes more rear involvement).
Susceptibility
- Balb/c
- DBA/1
- B10.RIII
- C57Bl/6
Literature/Support
- ArthritoMab™ Antibody Cocktail, Product Insert
- Whitepaper: For induction of arthritis in the Collagen Antibody Induced Arthritis (CAIA)model: a shorter, more synchronized alternative to the classic CIA model.
- Poster: ArthritoMab™ Antibody Cocktail: a cocktail of anti-collagen type II antibodies induce a synchronized model of Arthritis in just 12 days.
- Publication: Efficient promotion of collagen antibody induced arthritis (CAIA)using four monoclonal antibodies specific for the majorepitopes recognized in both collagen induced arthritisand rheumatoid arthritis. Nandukamar & Holmdahl Journal of Immunological Methods 304 (2005) 126 – 136
References/Citations:
Liao, K., Su, X., Lei, K., Liu, Z., Lu, L., Wu, Q., ... & Li, T. (2021) Sinomenine protects bone from destruction to ameliorate arthritis via activating p62Thr269/Ser272-Keap1-Nrf2 feedback loop.Biomedicine & Pharmacotherapy,135, 111195.
Maleitzke, T., Hildebrandt, A., Weber, J., Dietrich, T., Appelt, J., Jahn, D., ... & Keller, J. (2020). Proinflammatory and bone protective role of calcitonin gene-related peptide alpha in collagen antibody-induced arthritis. Rheumatology.
Cambré, I., Gaublomme, D., Schryvers, N., Lambrecht, S., Lories, R., Venken, K., & Elewaut, D. (2019). Running promotes chronicity of arthritis by local modulation of complement activators and impairing T regulatory feedback loops. Annals of the rheumatic diseases, 78(6), 787-795.
Gilis, E., Gaublomme, D., Staal, J., Venken, K., Dhaenens, M., Lambrecht, S., ... & Dumas, E. (2019). Deletion of Mucosa-Associated Lymphoid Tissue Lymphoma Translocation Protein 1 in Mouse T Cells Protects Against Development of Autoimmune Arthritis but Leads to Spontaneous Osteoporosis. Arthritis & Rheumatology (Hoboken, NJ), 71(12), 2005-2015
Schroeder, J., Ross, K., McIntosh, K., Jabber, S., Woods, S., Crowe, J., ... & Plevin, R. (2019). Novel protective role for MAP kinase phosphatase 2 in inflammatory arthritis. RMD open, 5(1), e000711.
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 & therapy,21(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 reports,8(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.
Prendergast, C. T., Patakas, A., Al-Khabouri, S., McIntyre, C. L., McInnes, I. B., Brewer, J. M., ... & Benson, R. A. (2018). Visualising the interaction of CD4 T cells and DCs in the evolution of inflammatory arthritis.Annals of the rheumatic diseases,77(4), 579-588.
Su, X., Li, T., Liu, Z., Huang, Q., Liao, K., Ren, R., ... & Zhou, H. (2018). Licochalcone A activates Keap1-Nrf2 signaling to suppress arthritis via phosphorylation of p62 at serine 349.Free Radical Biology and Medicine,115, 471-483.
Armaka, M., Ospelt, C., Pasparakis, M., & Kollias, G. (2018). The p55TNFR-IKK2-Ripk3 axis orchestrates arthritis by regulating death and inflammatory pathways in synovial fibroblasts.Nature Communications,9(1), 618.
Tang, X., Alasiri, M., Bamashmous, A., Aljahdali, B., Cao, F., Dibart, S., & Salih, E. (2018). The involvement of Kav001 in inhibition of LPS/P. gingivalis‐induced.Journal of cellular biochemistry,119(7), 6072-6079.
Kim, J. Y., Lim, K., Kim, K. H., Kim, J. H., Choi, J. S., & Shim, S. C. (2018). N-3 polyunsaturated fatty acids restore Th17 and Treg balance in collagen antibody-induced arthritis.PloS one,13(3), e0194331.
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
Pfeifle, R., Rothe, T., Ipseiz, N., Scherer, H. U., Culemann, S., Harre, U., ...& Haugg, B. (2017). Regulation of autoantibody activity by the IL-23–T H 17 axis determines the onset of autoimmune disease.Nature immunology,18(1), 104.
Neerinckx, B., Kollnberger, S., Shaw, J., & Lories, R. (2017). No evidence for a direct role of HLA-B27 in pathological bone formation in axial SpA.RMD open,3(1), e000451.
Alshammari, A., Patel, J., Al‐Hashemi, J., Cai, B., Panek, J., Huck, O., & Amar, S. (2017). Kava‐241 reduced periodontal destruction in a collagen antibody primed Porphyromonas gingivalis model of periodontitis.Journal of Clinical Periodontology,44(11), 1123-1132
Tang, X., & Amar, S. (2016). Kavain inhibition of LPS-induced TNF-α via ERK/LITAF.Toxicology Research,5(1), 188-196.
Tang, X., & Amar, S. (2016). Kavain Involvement in LPS‐Induced Signaling Pathways.Journal of Cellular Biochemistry,117(10), 2272-2280.
Tu, J., Zhang, Y., Kim, S., Wiebe, E., Spies, C. M., Buttgereit, F., ... & Zhou, H. (2016). Transgenic Disruption of Glucocorticoid Signaling in Osteoblasts Attenuates Joint Inflammation in Collagen Antibody–Induced Arthritis.The American Journal of Pathology,186(5), 1293-1301.
Shekhani, M. T., Forde, T. S., Adilbayeva, A., Ramez, M., Myngbay, A., Bexeitov, Y., ... & Adarichev, V. A. (2016). Collagen triple helix repeat containing 1 is a new promigratory marker of arthritic pannus.Arthritis Research & Therapy,18(1), 171.
Cheng, T. L., Lai, C. H., Shieh, S. J., Jou, Y. B., Yeh, J. L., Yang, A. L., ... & Ho, M. L. (2016). Myeloid thrombomodulin lectin-like domain inhibits osteoclastogenesis and inflammatory bone loss.Scientific Reports,6, 28340.
Banda, N. K., Acharya, S., Scheinman, R. I., Mehta, G., Coulombe, M., Takahashi, M., ...& Holers, V. M. (2016). Mannan-Binding Lectin–Associated Serine Protease 1/3 Cleavage of Pro–Factor D into Factor D In Vivo and Attenuation of Collagen Antibody-Induced Arthritis through Their Targeted Inhibition by RNA Interference–Mediated Gene Silencing.The Journal of Immunology, 1600719.
Grahnemo, L., Andersson, A., Nurkkala-Karlsson, M., Stubelius, A., Lagerquist, M. K., Svensson, M. N., ...& Islander, U. (2015). Trabecular bone loss in collagen antibody-induced arthritis.Arthritis research & therapy,17(1), 189.
Redelinghuys, P., Whitehead, L., Augello, A., Drummond, R. A., Levesque, J. M., Vautier, S., ... & Wright, J. (2015). MICL controls inflammation in rheumatoid arthritis.Annals of the rheumatic diseases, annrheumdis-2014.
Pineda, M. A., Al‐Riyami, L., Harnett, W., & Harnett, M. M. (2014). Lessons from helminth infections: ES‐62 highlights new interventional approaches in rheumatoid arthritis.Clinical & Experimental Immunology,177(1), 13-23
Moore, A. R., Allden, S., Bourne, T., Denis, M. C., Kranidioti, K., Okoye, R., ...& Shaw, S. (2014). Collagen II antibody-induced arthritis in Tg1278TNFko mice: optimization of a novel model to assess treatments targeting human TNFα in rheumatoid arthritis.Journal of translational medicine,12(1), 285.
References/Citations: | How the ArthritoMab™ Antibody Cocktail was used: |
| Fc receptor beta chain deficiency exacerbates murine arthritis in the anti-type II collagen antibody-induced experimental model. Ohtsubo-Yoshioka, M et al (2012) Mod. Rheum.DOI 10.1007/s10165-012-0749-z | Induced Arthritis in C57Bl/6 mice using 2 mg of ArthritoMab Antibody Cocktail and 100 ug LPS. |
| Pharmacological targeting reveals distinct roles for CXCR2/CXCR1 and CCR2 in a mouse model of arthritis. Min S. et al. Biochemical and biophysical research communications. 2010; 391(1):1080-6. | Induce arthritis in 8- and 10-week old BALB/c mice.On day 0, mice were injected intraperitoneally with 4 mg of ArthritoMab.On day 3, mice were boosted intraperitoneally with 50 ug of lipopolysacharide in 200 ul sterile PBS. |
| Apremilast, a novel PDE4 inhibitor, inhibits spontaneous production of tumour necrosis factor-alpha from human rheumatoid synovial cells and ameliorates experimental arthritis. McCann FE, et al. Arthritis Res Ther. 2010 Jun; 12(3):R107. | Induced arthritis experiments using six-week-old male BALB/c mice. |
| Pharmacological targeting reveals distinct roles for CXCR2/CXCR1 and CCR2 in a mouse model of arthritis. Soo-Hong Min et al., Biochemical and Biophysical Research Communications 391 (2010) 1080-1086. | Induce arthritis in Female BALB/c mice between 8 and 10 weeks of age.Each mouse received a 4mg intraperitoneal injection on day 0 and a 50ug boost of LPS on day 3. |
| The novel small molecule drug Rabeximod is effective in reducing disease severity of mouse models of autoimmune disorders M Hultqvist, K S Nandakumar, U Björklund, and R HolmdahlAnn Rheum Dis, Jan 2009; 68: 130 - 135. | Induce arthritis in BALB/c mice.On day 0, 100 mg/kg (2 mg/mouse) ofArithritoMab was injected to induce arthritis.At day 5 or 3 respectively, lipopolysacharide (LPS) was injected intraperitoneally (50 ug/mouse) to enhance the incidence. |
| Mast cell chymase contributes to the antibody response and the severity of autoimmune arthritis. Sofia E. Magnusson, Gunnar Pejler, Sandra Kleinau, and Magnus ÅbrinkFASEB J, Mar 2009; 23: 875 - 882. | Induce arthritis in genetically modified mice backcrossed to the arthritis-susceptible DBA/1 strain.Each mouse recieved a total of 4mg of ArthritoMab transferred intravenously in two consecutive days.On the fourth day, a 50ug boost of LPS was given by intraperitoneal injection. |
| Dominant-Negative Inhibitors of Soluble TNF Attenuate Experimental Arthritis without Suppressing Innate Immunity to Infection Jonathan Zalevsky et al.,J. Immunol., Aug 2007; 179: 1872 - 1883. | Induce arthritis in Male BALB/c mice.Each mouse recieved 25 mg/kg of ArthitoMab through i.v. injection on day 0 and a 2.5 mg/kg boost of LPS given by i.p. 72 h later. |
| PRECLINICAL EFFICACY OF XPROTM 1595, A BIOLOGIC DOMINANT-NEGATIVE INHIBITOR OF SOLUBLE TNF THAT BLOCKS INFLAMMATION WITHOUT SUPPRESSING INNATE IMMUNITY J. Zalevsky, P. Wong, C. O"Brien, and D.E. SzymkowskiAnn Rheum Dis, Jun 2006; 65: 142. |
How To Use
Applications
- In vivo: induce disease in the collagen antibody induced arthritis model
- bind collagen in vivo
- impair cartilage formation by chondrocytes in vitro
- inhibit assembly of CII in vitro
- inhibit collagen fibrillogenesis in vitro
- Administer antibody cocktail on day 0*
- Boost with LPS on day 3
- Terminate on day 12
Download a whitepaper on using the CAIA model as an alternative to CIA or K/BxN serum transfer models.
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