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      Colony variability under the spotlight in animal models of arthritis

      editorial
      Author(s): 1 ,
      Publication date (Electronic):
      Journal: Arthritis Research & Therapy
      Publisher: BioMed Central

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          Abstract

          A recent article by Farkas and colleagues, published in Arthritis Research & Therapy, is from the laboratory of Dr Tibor Glant and his research team in Chicago, who have investigated in considerable depth the immunopathology of experimental arthritis induced by the major cartilage component proteoglycan aggrecan in an animal model that mimics many features of human rheumatoid arthritis and ankylosing spondylitis. This present report takes our understanding a significant step forward by questioning whether genetic drift in distinct colonies of the same inbred strains of mice has an impact on the parity between data published by different laboratories.

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          The mouse ascending: perspectives for human-disease models.

          Nadia Rosenthal, Steve Brown (2007)
          The laboratory mouse is widely considered the model organism of choice for studying the diseases of humans, with whom they share 99% of their genes. A distinguished history of mouse genetic experimentation has been further advanced by the development of powerful new tools to manipulate the mouse genome. The recent launch of several international initiatives to analyse the function of all mouse genes through mutagenesis, molecular analysis and phenotyping underscores the utility of the mouse for translating the information stored in the human genome into increasingly accurate models of human disease.
          Article 0 comments Cited 140 times – based on 0 reviews     Review now
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            Immunopathogenesis of collagen arthritis.

            David Brand, Edward Rosloniec, J. Kang (2003)
            Collagen-induced arthritis (CIA) is an animal model of autoimmunity that has been studied extensively because of its similarities to rheumatoid arthritis (RA). CIA is induced in genetically susceptible strains of mice by immunization with type II collagen (CII), and both T cell and B cell immunity to CII are required for disease manifestation. Like RA, CIA is primarily an autoimmune disease of articular joints and susceptibility to CIA is linked to specific class II molecules of the major histocompatibility complex (H-2(r) and H-2(q)). Recently, it was demonstrated that transgenic expression of HLA-DR1 (*0101) or DR4 (*0401) molecules associated with susceptibility to RA also conferred susceptibility to CIA in the mouse model. The T cell response to CII has been extensively characterized in both the DR transgenic and naturally susceptible mouse strains, including the antigenic determinants recognized, the role of post transcriptional modifications of these determinants in the pathogenic T cell response, and the cytokines produced. Like most class II-mediated autoimmune diseases, the cytokine production of CII-specific T cells reflects a Th1 phenotype of the autoimmune response. While the direct role of T cells in the pathogenesis of CIA is unclear, the B cell response in terms of anti-CII immunoglobulin is critical to the development of the disease. This response, predominated by the IgG2 isotype, requires the activation of the complement cascade for the development of CIA. In recent years, the pathogenesis of this model has been studied extensively and the CIA model is proving to be a valuable asset for the design of new immunotherapeutics for the potential treatment of RA and other autoimmune diseases.
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              Proteoglycan-induced arthritis: immune regulation, cellular mechanisms, and genetics.

              Tibor Glant, Alison Finnegan, Katalin Mikecz (2002)
              Rheumatoid arthritis is probably the least understood systemic autoimmune disease, and it affects approximately 1% of the human population. Several lines of evidence indicate that the effector mechanism, which initially attacks small joints, is T-cell driven. As a result, an aggressive synovial pannus develops, which destroys articular cartilage and bone, leading to massive ankylosis and deformities of peripheral joints. The disease has a progressive character, with the involvement of more and more joints. Although the target organ is the synovial joint, there is no clear evidence that any macromolecule of cartilaginous tissues, bone, or synovium, could be a preferential autoantigen. There are numerous rodent models that simulate some or many of the clinical, immunological, or histopathological features of the disease. Recently, it has become a strong working hypothesis that MHC and non-MHC genetic components share loci that are common in various autoimmune diseases, and in corresponding animal models. The most relevant animal models of rheumatoid arthritis appear to be those induced by cartilage matrix components such as type II collagen or proteoglycan aggrecan. This review summarizes our current knowledge of cartilage proteoglycan (aggrecan)-induced arthritis in mice.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Arthritis Res Ther
                Title: Arthritis Research & Therapy
                Publisher: BioMed Central
                ISSN (Print): 1478-6354
                ISSN (Electronic): 1478-6362
                Publication date (Print): 2009
                Publication date (Electronic): 30 April 2009
                Volume: 11
                Issue: 2
                Page: 110
                Affiliations
                [1 ]Musculoskeletal Research Group, Institute of Cellular Medicine, Newcastle University, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK
                Article
                Publisher ID: ar2653
                DOI: 10.1186/ar2653
                PMC ID: 2688192
                PubMed ID: 19439055
                SO-VID: 0726e7c9-e155-4d4c-8167-33ed77d6a0cf
                Copyright © Copyright © 2009 BioMed Central Ltd
                History
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                Subject: Editorial

                ScienceOpen disciplines: Orthopedics
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                ScienceOpen disciplines: Orthopedics

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