Collagen‐Induced Arthritis

Rosloniec, Edward F.; Cremer, Michael A.; Kang, Andrew H.; Myers, Linda K.

doi:10.1002/0471142735.im1505s20

Cited by 99 publications

(100 citation statements)

References 22 publications

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“…Briefly, mice were either left naive, immunized in the tail s.c. with 100 g of type II chicken collagen (CII; Sigma-Aldrich) dissolved in 10 mM acetic acid and emulsified in IFA (Sigma-Aldrich) containing 5 mg/ml H37 RA heat-killed mycobacteria (CFA; Difco Laboratories), or immunized with 10 mM acetic acid emulsified in CFA. Mice were monitored for limb erythema and swelling and paws measured (each paw recorded individually; four measurements per mouse) with calipers two to three times per week (4026F; Mitutoyo) (29,30). All mouse studies were reviewed and approved by the University of Iowa Animal Care and Use Committee.…”

Section: Mice/cia Inductionmentioning

confidence: 99%

A Costimulatory Function for T Cell CD40

Munroe

Bishop

2007

The Journal of Immunology

100

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CD40 plays a significant role in the pathogenesis of inflammation and autoimmunity. B cell CD40 directly activates cells, which can result in autoantibody production. T cells can also express CD40, with an increased frequency and amount of expression seen in CD4+ T lymphocytes of autoimmune mice, including T cells from mice with collagen-induced arthritis. However, the mechanisms of T cell CD40 function have not been clearly defined. To test the hypothesis that CD40 can serve as a costimulatory molecule on T lymphocytes, CD40+ T cells from collagen-induced arthritis mice were examined in parallel with mouse and human T cell lines transfected with CD40. CD40 served as effectively as CD28 in costimulating TCR-mediated activation, including induction of kinase and transcription factor activities and production of cytokines. An additional enhancement was seen when both CD40 and CD28 signals were combined with AgR stimulation. These findings reveal potent biologic functions for T cell CD40 and suggest an additional means for amplification of autoimmune responses.

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Section: Mice/cia Inductionmentioning

confidence: 99%

A Costimulatory Function for T Cell CD40

Munroe

Bishop

2007

The Journal of Immunology

100

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“…CII was solubilized in 0.01M acetic acid at a concentration of 4 mg/ml and emulsified with an equal volume of Freund's complete adjuvant (CFA) containing 4 mg/ml of Mycobacterium tuberculosis (Ministry of Agriculture, Fisheries, and Food, Weybridge Surrey, UK) (19). Each mouse received from 25-100 g of CII emulsified in CFA, administered intradermally at the base of the tail.…”

Section: Methodsmentioning

confidence: 99%

“…The incidence and severity of arthritis were determined by visually examining each forepaw and hindpaw and scoring them on a scale of 0-4 as described previously (19). Scoring was conducted by 2 examiners, one of whom was unaware of the identity of the treatment groups.…”

Section: Methodsmentioning

confidence: 99%

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Efficacy of modified recombinant type II collagen in modulating autoimmune arthritis

Myers¹,

Tang²,

Brand³

et al. 2004

Arthritis & Rheumatism

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Objective. Previous studies have shown that an analog peptide of the immunodominant T cell determinant of type II collagen (CII), i.e., CII (N 263 , D 266 ), was able to suppress the immune response to CII and the development of arthritis in DR1-transgenic mice. The present study tested the hypothesis that introduction of the same amino acid substitutions into fulllength CII might improve the efficacy of the mutant collagen in achieving suppression of autoimmune arthritis.Methods. Using recombinant technology, fulllength CII was modified, while the native conformation was retained. Two point mutations were introduced within the immunodominant T cell determinant to convert the F 263 to N and E 266 to D, using a baculovirus expression system that has previously been utilized in the production of recombinant CII (rCII).Results. The mutant rCII(N 263 , D 266 ) was capable of reducing the incidence and severity of arthritis as well as the antibody response to CII when administered to DR1-transgenic mice that display susceptibility to collagen-induced arthritis. More importantly, it was significantly more effective than the synthetic analog peptide, CII Conclusion. These findings describe a promising specific immunotherapy for patients with DR1-mediated autoimmunity to CII.Collagen-induced arthritis (CIA) is a tissuespecific autoimmune disease that develops in susceptible animals when they are immunized with type II collagen (CII). It is characterized by inflammation of synovial joints and possesses many characteristics of human rheumatoid arthritis (RA) (1-3). Susceptibility to CIA is dependent on the class II immune response genes of the major histocompatibility complex (MHC) (4-6) and the development of a strong immune response to CII. We recently showed that mice transgenic for the human immune response genes DRB1*0101 (DR1) or DRB1*0401 (DR4), which are susceptibility markers for human RA, are also highly susceptible to CIA (7-9). The susceptibility of DR1-transgenic mice to CIA offers the opportunity to study the role of the human RA susceptibility marker, DR1, in the selection of arthritogenic T cells, in an easily controlled environment.The immunodominant peptide recognized by T cells from DR1-transgenic mice was identified as CII 260-267 (8). Moreover, an analog peptide, CII (N 263 , D 266 ), which has 2 critical substitutions, was developed and shown to be capable of preventing disease when administered as a coimmunogen with CII (10). There are cogent reasons to believe that incorporation of the analog substitutions into full-length CII might improve the efficacy of this altered peptide ligand (APL) in suppression of arthritis. Native CII is immunologically more potent than chemically synthesized peptides. The potency of the immune response against the CII molecule may be mediated through maintenance of the triple-helix conformation or through posttranslational modifications such as hydroxylation and glycosylation of hydroxylysine residues (11-13).

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“…9 The resulting emulsion was injected intradermally into the base of the tail. Each mouse received a total volume of 0Á05 ml containing 100 lg Mycobacterium tuberculosis and 100 lg of antigen.…”

Section: Immunizationmentioning

confidence: 99%

Molecular characterization of an arthritogenic collagen peptide interacting with I‐A^r

Sakurai

Tang²,

Rosloniec

et al. 2005

Immunology

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SummaryCollagen-induced arthritis (CIA) is an autoimmune arthritis that can be elicited by the immunization of genetically susceptible strains of mice with type II collagen (CII). We have analysed the molecular interactions that occur between an arthritogenic T-cell determinant CII (442-457) and the murine class II susceptibility allele I-A r . To determine which amino acid residues within the CII (442-457) sequence are responsible for binding to I-A r , a soluble I-A r : IgG2aFc fusion protein-peptide binding assay was developed. Various concentrations of analogue peptides were tested for their ability to compete with biotinylated CII (607-622) for binding to I-A r , thereby establishing a relative comparison of the binding affinities among these analogues. Analogue peptides with substitutions at positions 447 (Ala fi Val), 448 (Gly fi Ala) and 451 (Gly fi Ala) bound poorly to the I-A r molecule. These data suggest that positions 447, 448 and 451 on CII are the major anchor points to I-A r molecules. In cytokine assays, only substitutions within positions 445-454 decreased the interferon-c production by T cells. These data narrow the core of the arthritogenic T-cell determinant to CII (445-454). Identification of the molecular interactions involved in T-cell recognition of CII should lead to antigenspecific means of inhibiting autoimmune arthritis.

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Collagen‐Induced Arthritis

Cited by 99 publications

References 22 publications

A Costimulatory Function for T Cell CD40

A Costimulatory Function for T Cell CD40

Efficacy of modified recombinant type II collagen in modulating autoimmune arthritis

Molecular characterization of an arthritogenic collagen peptide interacting with I‐A^r

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Collagen‐Induced Arthritis

Cited by 99 publications

References 22 publications

A Costimulatory Function for T Cell CD40

A Costimulatory Function for T Cell CD40

Efficacy of modified recombinant type II collagen in modulating autoimmune arthritis

Molecular characterization of an arthritogenic collagen peptide interacting with I‐Ar

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Molecular characterization of an arthritogenic collagen peptide interacting with I‐A^r