The Immunogenetic Basis of Collagen Induced Arthritis in Mice: An Experimental Model for the Rational Design of Immunomodulatory Treatments of Rheumatoid Arthritis

Nabozny, Gerald H.; David, Chella S.

doi:10.1007/978-1-4615-2427-4_6

Cited by 14 publications

(3 citation statements)

References 47 publications

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“…Inflammation of joint regions was observed in the affected paws of CII-immunized mice as described previously [16][17][18]. Since IgG-type anti-CII antibodies were positive only in this immunized group, the generation of antibodies that cross-react with collagen in the region is thought to be one of the causes of this inflammation [16].…”

Section: Discussionmentioning

confidence: 99%

“…Collagen-induced arthritis (CIA) is an experimental model of chronic arthritis and/or RA, a proliferative disorder of connective tissues [16][17][18]. In the present study, we investigated whether increases in MCs and chymase were correlated with the matrix turnover in the fibroproliferative paws associated with type II collagen (CII)-induced arthritis in mice.…”

Section: Introductionmentioning

confidence: 99%

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Increases in mast cells and chymase in fibroproliferative paws of collagen-induced arthritic mice

Kakizoe

Kobayashi

et al. 1999

Inflamm. res.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Increases in mast cells and chymase in fibroproliferative paws of collagen-induced arthritic mice

Kakizoe

Kobayashi

et al. 1999

Inflamm. res.

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“…It has also been shown that the resistance of autoreactive B cells to apoptosis in RA is conferred by the up-regulation of Bcl-x L expression (9). Collageninduced arthritis (CIA) is an experimental model of autoimmune disease that shares many of the histologic and immunilogic characteristics found in human RA (10,11). Both cellular and humoral immune responses to type II collagen (CII) are involved in the pathogenesis of CIA.…”

mentioning

confidence: 99%

Overexpression of BclXL in B Cells Promotes Th1 Response and Exacerbates Collagen-Induced Arthritis

Zheng

Marinova

Switzer

et al. 2007

The Journal of Immunology

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B cells play a pathogenic or regulatory role in many autoimmune diseases through production of autoantibodies, cytokine production, and Ag presentation. However, the mechanisms that regulate these B cell functions under different autoimmune settings remain unclear. In the current study, we found that when B cells overexpress an antiapoptotic gene, BclXL, they significantly increased production of IFN-γ and enhanced Th1 response. Consistently, Bcl-xL transgenic mice developed more severe and sustained collagen-induced arthritis due to the enhanced Th1 response. The production of autoantibodies in BclXL transgenic mice was comparable to that in wild-type mice. Thus, our results indicate a novel role of BclXL in regulating B cell functions and immune responses. In patients with rheumatoid arthritis, arthritogenic B cells often up-regulate BclXL expression, which may not only render B cells resistant to apoptosis but also alter the ability of the autoreactive B cells to produce cytokines and modulate the inflammatory response. This may have therapeutic implications if BclXL expression can be down-regulated in autoreactive B cells.

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Autoimmune Disease: Animal Models

Williams

2010

Encyclopedia of Life Sciences

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Animal models are used for the study of a number of human autoimmune diseases, including multiple sclerosis, diabetes, rheumatoid arthritis and systemic lupus erythematosis. Induced, spontaneous and genetically manipulated animal models can be described in terms of their parallels to human disease and as tools for the development of potential therapies. Studies in animal models have led to a number of important discoveries which have increased our understanding of the pathogenesis of autoimmune disease, including the roles played by regulatory T cells and T H 17 cells. In addition, important therapeutic advances have emerged as a result of studies of immune intervention in animal models of autoimmunity. For example, Tumour necrosis factor (TNF) blocking drugs, which are widely used for the treatment of rheumatoid arthritis, were developed following pre‐clinical testing in animal models. Key Concepts: Animal models may be either spontaneously occurring or induced as a result of genetic manipulation or immunisation with a self‐antigen. No animal model completely mimics human disease. Animal models can be used to test novel therapeutic concepts and to understand mechanisms of drug action. The use of transgenic and knockout strains facilitates the identification of key genes that contribute to disease susceptibility.

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The Immunogenetic Basis of Collagen Induced Arthritis in Mice: An Experimental Model for the Rational Design of Immunomodulatory Treatments of Rheumatoid Arthritis

Cited by 14 publications

References 47 publications

Increases in mast cells and chymase in fibroproliferative paws of collagen-induced arthritic mice

Increases in mast cells and chymase in fibroproliferative paws of collagen-induced arthritic mice

Overexpression of BclXL in B Cells Promotes Th1 Response and Exacerbates Collagen-Induced Arthritis

Autoimmune Disease: Animal Models

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