Collagen-induced arthritis in rats. Examination of the epitope specificities of circulating and cartilage-bound antibodies produced by outbred and inbred rats using cyanogen bromide-derived peptides purified from heterologous and homologous type II collagens.

Cremer, Michael A.; Terato, Kuniaki; Watson, William C.; Griffiths, Marie; Townes, Alexander S.; Kang, An-Jing

doi:10.4049/jimmunol.149.3.1045

Cited by 20 publications

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Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1^av1 haplotype

Griffiths

Cannon

Leonard

et al. 1993

Arthritis & Rheumatism

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Objective. To test for genetic differences in susceptibility to homologous (rat) type I1 collagen-induced arthritis (RII-CIA).Methods. Nine inbred and RT1-congenic rat strains were immunized with native rat type I1 collagen and evaluated for arthritis and IgG anti-RII serum antibody titers.Results. Only RTla"' strains developed a high incidence of severe RII-CIA and high titers of IgG anti-RII serum antibody. Rats having RII-CIAresistant haplotypes, RTI".".' (which are known to develop CIA after immunization with heterologous type I1 collagen), were shown to also be susceptible to passive transfer of CIA with immune serum concentrates. Clinical expression of RII-CIA was down-regulated by non-RT1 genes of BN origin. No strong gender differences in anti-RII autoimmune responses were observed.Conclusion. Arthritogenic, autoimmune reactivity to homologous RII is under strict genetic control but occurs readily in RT1"" rats. Collagen-induced arthritis (CIA) is an experimentally induced model of chronic arthritis that hasFrom The Research Service, Salt Lake City Veteran Affairs Medical Center, and the Division of Rheumatology, University of Utah Medical School, Salt Lake City, Utah.Supported been studied in rats, mice, and primates. Joint inflammation in CIA is due to the generation of collagenreactive T cells and complement-binding, IgG anticollagen antibodies that cross-react with autologous type I1 collagen in joint cartilage (1,2). Several gene products influence the susceptibility of an individual rat to CIA (3-5). Of primary importance are the class I1 molecules that are encoded within the major histocompatibility complex (RTl), and that bind collagen peptides for presentation to T cells by antigen processing cells (5). Equally important are the non-major histocompatibility complex-encoded (non-MHC-encoded), T cell antigen receptor (TCR) molecules, which dictate the strength of interaction between specific T cells and each of the multiple immunogenic peptide fragments of type 11 collagen (6).CIA is commonly induced by immunization with heterologous, native type I1 collagen extracted from the articular cartilage of diverse species including bovine, chick, deer, porcine, and human. The minor, species-specific differences in amino acid sequence that exist among these very conserved molecules are readily detected by the rat immune system and cause an RTl-restricted variability in strain susceptibility to CIA induction by type I1 collagens of different origins (7,8).In this study we analyzed the response of several inbred and RTI-congenic rat strains to immunization with homologous rat type I1 collagen (RII). Of those tested, only one MHC haplotype, RTI"", was associated with a high degree of susceptibility to RII-CIA, although the other haplotypes that were tested are known to promote the induction of CIA by immunization with heterologous type I1 collagens. The results show that MHC-encoded genes determine the

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Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1^av1 haplotype

Griffiths

Cannon

Leonard

et al. 1993

Arthritis & Rheumatism

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Collagen‐Induced Arthritis Mouse Model

Rosloniec

Whittington²,

Proslovsky³

et al. 2021

Current Protocols

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The collagen-induced arthritis mouse model is a widely studied autoimmune model of rheumatoid arthritis. In this model, autoimmune arthritis is induced by immunization of genetically susceptible strains of mice with type II collagen emulsified in complete Freund's adjuvant. This article describes the steps necessary for the acquisition, handling, and preparation of CII, in addition to the selection of mouse strains, proper immunization technique, and methods for evaluation of the incidence and severity of the autoimmune arthritis. In this model, the first signs of arthritis appear approximately 21 to 28 days after immunization. The protocols in this article should provide the investigator with all the necessary information required to reproducibly induce a high incidence of CIA in genetically susceptible strains of mice, and to critically evaluate the pathology of the disease.

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MED and PSACH COMP mutations affect chondrogenesis in chicken limb bud micromass cultures

Roman‐Blas¹,

Dion²,

Seghatoleslami³

et al. 2010

Journal Cellular Physiology

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Mutations in cartilage oligomeric matrix protein (COMP) cause pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED). We studied the effects of over-expression of wild type and mutant COMP on early stages of chondrogenesis in chicken limb bud micromass cultures. Cells were transduced with RCAS virus harboring wild type or mutant (C328R, PSACH; T585R, MED) COMP cDNAs and cultured for 3, 4, and 5 days. The effect of COMP constructs on chondrogenesis was assessed by analyzing mRNA and protein expression of several COMP binding partners. Cell viability was assayed, and evaluation of apoptosis was performed by monitoring caspase 3 processing. Over-expression of COMP, and especially expression of COMP mutants, had a profound affect on the expression of syndecan 3 and tenascin C, early markers of chondrogenesis. Over-expression of COMP did not affect levels of type II collagen or matrilin-3; however, there were increases in type IX collagen expression and sulfated proteoglycan synthesis, particularly at day 5 of harvest. In contrast to cells over-expressing COMP, cells with mutant COMP showed reduction in type IX collagen expression and increased matrilin 3 expression. Finally, reduction in cell viability, and increased activity of caspase 3, at days 4 and 5, were observed in cultures expressing either wild type or mutant COMP. MED, and PSACH mutations, despite displaying phenotypic differences, demonstrated only subtle differences in their cellular viability and mRNA and protein expression of components of the extracellular matrix, including those that interact with COMP. These results suggest that COMP mutations, by disrupting normal interactions between COMP and its binding partners, significantly affect chondrogenesis.

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Collagen-induced arthritis in rats. Examination of the epitope specificities of circulating and cartilage-bound antibodies produced by outbred and inbred rats using cyanogen bromide-derived peptides purified from heterologous and homologous type II collagens.

Cited by 20 publications

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Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1^av1 haplotype

Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1^av1 haplotype

Collagen‐Induced Arthritis Mouse Model

MED and PSACH COMP mutations affect chondrogenesis in chicken limb bud micromass cultures

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Collagen-induced arthritis in rats. Examination of the epitope specificities of circulating and cartilage-bound antibodies produced by outbred and inbred rats using cyanogen bromide-derived peptides purified from heterologous and homologous type II collagens.

Cited by 20 publications

References 0 publications

Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1av1 haplotype

Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1av1 haplotype

Collagen‐Induced Arthritis Mouse Model

MED and PSACH COMP mutations affect chondrogenesis in chicken limb bud micromass cultures

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Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1^av1 haplotype

Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1^av1 haplotype