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ArthritoMab™ Antibody Cocktail for C57BL/6

Catalog Number: 
CIA-MAB-2C
Qty/Size: 
50 mg

ArthritoMab antibody cocktail from MD Bioproducts

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International: +41-44 986 2628

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download arthritomab data pack and protocol optimization guideArthritoMab™ Antibody Cocktail is a reformulated cocktail of 4 monoclonal antibodies for the induction of arthritis as an alternative to the widely used collagen-induced arthritis (CIA) model. Many transgenic strains of mice are on a C57BL/6 background. However this strain is refractory to arthritis induction either by CIA or CAIA. Traditionally to overcome this in the CAIA model an increased dose of antibody cocktail is given. This reformulated cocktail of antibodies is optimized for production of arthritis in C57BL/6, inducing arthritis with lower doses of antibody. This new formulation can also be used in other strains of mouse, which traditionally require greater amounts of cocktail.

Download a data pack to learn more about inducing arthritis in C57 strains.

Overview

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.

 

ArthritoMab antibody cocktail for induction in C57Bl/6 strains

Comparison

 ArthritoMab™Competitor

Epitopes Recognized

CB11, CB10, CB8CB11 only
Disease ProgressionSteady & ControlledRapid & Severe
Paw involvementConsistent & Predominantely rearVariable & unpredictable
Amount required for C57Bl/62 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

Data/Specifications: 

Epitope specificity

The classic CIA model is mediated by autoantibodies which bind to type II collagen and complement. In mice as well as human RA patients, the antibody response that best correlates with disease is directed against the C1, J1 and U1 epitopes. The ArthritoMab™ arthritogenic cocktail of 4 monoclonal antibodies binds to these well-defined epitopes C11b, J1, D3 and U1, which are spread over the entire CII (CB8, CB10 and CB11 fragments). This possibly encourages better immune complex formation on the cartilage surface for the initiation of arthritis and produces consistent and predictable disease in all 4 paws (with predominance for the rear). Competitor products only recognize CB11, which produces variable disease that can contribute to unpredictable involvement in the paws (sometimes more front paw involvment and other times more rear involvement).

epitope specificity of Arthritomab antibody cocktial for inducing arthritis 

 

Susceptibility 

  • Balb/c
  • DBA/1
  • B10.RIII
  • C57Bl/6
Histopathology:
Similar features to the CIA model with only 2 mg antibody in C57Bl/6JN
histology in C57 using 2 mg Arthritomab antibody cocktail for arthritis induction

Literature/Support

Literature/Support: 

 

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 & 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.

 

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 diseases77(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 Medicine115, 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 communications9(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 biochemistry119(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 one13(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 immunology18(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 open3(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 periodontology44(11), 1123-1132

 

Tang, X., & Amar, S. (2016). Kavain inhibition of LPS-induced TNF-α via ERK/LITAF. Toxicology research5(1), 188-196.

 

Tang, X., & Amar, S. (2016). Kavain Involvement in LPS‐Induced Signaling Pathways. Journal of cellular biochemistry117(10), 2272-2280.

 

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 & therapy18(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 reports6, 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 & therapy17(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 Immunology177(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 medicine12(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-zInduced 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 Holmdahl Ann Rheum Dis, Jan 2009; 68: 130 - 135.
Induce arthritis in BALB/c mice. On day 0, 100 mg/kg (2 mg/mouse) of ArithritoMab 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 Åbrink FASEB 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. Szymkowski Ann Rheum Dis, Jun 2006; 65: 142.
 

 

 

 

 

How To Use

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
For the Induction of Arthritis in the Collagen Antibody Induced Arthritis Model:
  1. Administer antibody cocktail on day 0*
  2. Boost with LPS on day 3
  3. Terminate on day 12
*Amount of cocktail will vary depending on animal source and strain, housing conditions, feed and water. Each lab must optimize for their own conditions. 

Download a whitepaper on using the CAIA model as an alternative to CIA or K/BxN serum transfer models.