Collagen induced arthritis as an experimental model for rheumatoid arthritis

Holmdahl, Rikard; Andersson, Mikael; Goldschmidt, Tom; Jansson, Liselotte; Karlsson, Mikael C. I.; Malmström, Vivianne; Mo, John

doi:10.1111/j.1699-0463.1989.tb00446.x

Cited by 103 publications

(72 citation statements)

References 66 publications

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“…The susceptibility and resistance of DBA͞1j and SWR͞j, respectively, to the induction of CIA is well documented (9,10,15). As with previously published data, the DBA͞1j mice in these experiments had an incidence of 100% whereas the SWR͞j mice were completely resistant (0% incidence).…”

Section: Discussionmentioning

confidence: 99%

“…Genetic crosses between susceptible and resistant inbred mouse strains have demonstrated that CIA is inherited in most inbred strains as a polygenic, dominant trait (9,10). Several investigators have explored the role of the murine major histocompatibility complex (Mhc or H-2) in CIA development by immunization of congenic and inbred strains with heterologous and homologous CII (11)(12)(13)(14).…”

mentioning

confidence: 99%

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Localization of non-Mhccollagen-induced arthritis susceptibility loci in DBA/1j mice

McIndoe

Bohlman

Chi

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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One approach to understanding common human diseases is to determine the genetic defects responsible for similar diseases in animal models and place those defective genes in their corresponding biochemical pathways. Our laboratory is working with an animal model for human rheumatoid arthritis called collagen-induced arthritis (CIA). We are particularly interested in determining the location of disease-predisposing loci. To that end, we performed experiments to localize susceptibility loci for CIA in an F2 cross between the highly susceptible mouse strain DBA͞1j and the highly resistant mouse strain SWR͞j. Specifically, a quantitative trait locus analysis was performed to localize regions of the mouse genome responsible for susceptibility͞severity to CIA. One susceptibility locus, Cia1 in the major histocompatibility locus, had been identified previously. Two additional loci were detected in our analysis that contribute to CIA severity (Cia2, Cia3) on chromosomes 2 and 6. A third locus was detected that contributes to the age of onset of the disease. This locus (Cia4) was located on chromosome 2 and was linked to the same region as Cia2. Determining the identity of these loci may provide insights into the etiology of human rheumatoid arthritis.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Localization of non-Mhccollagen-induced arthritis susceptibility loci in DBA/1j mice

McIndoe

Bohlman

Chi

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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“…Arthritis is induced in susceptible strains of rats and mice by immunisation with type II collagen in incomplete Freund's adjuvant (IFA) or complete Freund's adjuvant (CFA), respectively (Holmdahl et al, 1989;Trentham, 1982). Both T helper (Th) 1 and (Th17) responses are induced in CIA, but Th17 cells appear to play the dominant pathological role (Murphy et al, 2003).…”

Section: Models Commonly Used For Drug Testing (A) Collagen-induced Amentioning

confidence: 99%

Animal models of rheumatoid arthritis: How informative are they?

McNamee

Williams

Seed

2015

European Journal of Pharmacology

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Animal models of arthritis are widely used to de-convolute disease pathways and to identify novel drug targets and therapeutic approaches. However, the high attrition rates of drugs in Phase II/III rates means that a relatively small number of drugs reach the market, despite showing efficacy in pre-clinical models. There is also increasing awareness of the ethical issues surrounding the use of animal models of disease and it is timely, therefore, to review the relevance and translatability of animal models of arthritis. In this paper we review the most commonly used animal models in terms of their pathological similarities to human rheumatoid arthritis as well as their response to drug therapy. In general, the ability of animal models to predict efficacy of biologics in man has been good. However, the predictive power of animal models for small molecules has been variable, probably because of differences in the levels of target knockdown achievable in vivo.3

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“…CIA is elicited through intradermal injection of chick or bovine type II collagen (CII) in the presence of Freund's complete adjuvant into genetically susceptible mice [56]. In initial studies, i.p.…”

Section: Mechanistic Lessons From Animal Modelsmentioning

confidence: 99%

TNFα blockade in human diseases: Mechanisms and future directions

Wong

Ziring

Korin

et al. 2008

Clinical Immunology

255

162

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Tumor necrosis factor-alpha (TNFα) antagonists have shown remarkable efficacy in a variety of immune-mediated inflammatory diseases (IMIDs). Therapeutic scope and limitations of these agents are reviewed in a recently published article in the Journal. In spite of their therapeutic popularity, little is known about their modes of action in vivo and factors that limit their scope of therapeutic use. Intriguingly, while all TNFα antagonists including blocking antibodies and soluble receptors are effective in certain IMIDs, only anti-TNFα antibodies are effective in other IMIDs. Early efforts at understanding how TNFα antagonists act in IMIDs centered on their ability to neutralize soluble TNFα or to block TNF receptors from binding to their ligands. Subsequent studies suggested a role of complement-mediated lysis or antibody-dependent cell cytotoxicity in their therapeutic effects. More recent models postulate that TNFα blockers may act by affecting intracellular signaling, with the end result being a hastened cell cycle arrest, apoptosis, suppression of cytokine production, or improved Treg cell function. TNFα antagonists can also modulate the functions of myofibroblasts and osteoclasts, which might explain how TNFα antagonists reduce tissue damage in chronic IMIDs. Focusing on the human therapeutic experience, this analytical review will review the biology of mechanisms of action, the limiting factors contributing to disease restriction in therapeutic efficacy, and the mechanism and frequency of treatment-limiting adverse responses of TNFα antagonists. It is hoped that the overview will address the needs of clinicians to decide on optimal use, spur clinical innovation, and incite translational researchers to set priorities for in vivo human investigations.

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Collagen induced arthritis as an experimental model for rheumatoid arthritis

Cited by 103 publications

References 66 publications

Localization of non-Mhccollagen-induced arthritis susceptibility loci in DBA/1j mice

Localization of non-Mhccollagen-induced arthritis susceptibility loci in DBA/1j mice

Animal models of rheumatoid arthritis: How informative are they?

TNFα blockade in human diseases: Mechanisms and future directions

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