Native type II collagen-induced arthritis in the rat. I. Incidence and humoral response to collagen.

Morgan, K; Clague, R B; Shaw, Mary J.; Holt, P. J.

doi:10.1136/ard.39.3.285

Cited by 64 publications

(20 citation statements)

References 13 publications

(15 reference statements)

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“…This discrepancy may be related to differences in immunoglobulin class, as we were detecting only IgG antibody, or the use of different techniques for estimation, or differences in case selection. Human serum IgG antibody levels to type TT collagen are relatively low when compared to the IgG antibody levels in experimental animals immunised with native collagen (Clague et al, 1979;Morgan et al, in press). There was a significant correlation between the serum IgG antibody levels to native type I and type rl collagens.…”

Section: Discussionmentioning

confidence: 96%

Incidence of serum antibodies to native type I and type II collagens in patients with inflammatory arthritis.

Clague¹,

Shaw²,

Holt³

1980

Annals of the Rheumatic Diseases

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SUMMARY Using a new solid-phase double-antibody radioimmunoassay we have determined the incidence of serum IgG antibodies to native bovine type I and type II collagens in patients with rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis. Raised serum IgG antibody levels to native type I collagen were present in 49 % of patients with RA, 30 % with AS, and none of the patients with psoriatic arthritis. Raised serum IgG antibody levels to native type II collagen were present in 42% of patients with RA, 30 % with AS, and none of the patients with psoriatic arthritis. In rheumatoid arthritis there was a lack of correlation between IgG antibody levels to collagen and the erythrocyte sedimentation rate, IgG rheumatoid factor, and circulating immune complexes measured by the Clq-binding activity. In ankylosing spondylitis IgG antibody levels to native type II collagen were raised only in patients with peripheral joint involvement. The significance of IgG anticollagen antibodies is not certain, but parallels with rheumatoid factor are discussed.

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Section: Discussionmentioning

confidence: 96%

Incidence of serum antibodies to native type I and type II collagens in patients with inflammatory arthritis.

Clague¹,

Shaw²,

Holt³

1980

Annals of the Rheumatic Diseases

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“…Rosenwasser et al (22) found that lymphocytes from nization with other types of collagen evoked lower levels of both cell-mediated and humoral immunity to the respective immunogens (2,27). Under the conditions used for immunization in the mouse, however, denatured type II collagen was capable of inducing both cell-mediated and humoral responses of comparable magnitudes to those seen when native type II collagen was the immunogen.…”

Section: Methodsmentioning

confidence: 99%

Nature and specificity of the immune response to collagen in type II collagen-induced arthritis in mice.

Stuart¹,

Townes²,

Kang³

1982

J. Clin. Invest.

169

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A B S T R A C T To determine the role of collagen-immunity in the development of collagen-induced arthritis, DBA/1 mice were immunized with type II collagen and observed for the development of polyarthritis. 96% of the mice immunized with native type II collagen developed inflammatory arthritis between 4 and 5 wk after primary immunization. Immunization with denatured type II collagen in exactly the same manner was not effective in inducing arthritis. Cell-mediated immunity in arthritic mice was assessed by measuring [3H]thymidine incorporation by mononuclear cells cultured in the presence of collagen. The maximal proliferative response to collagen occurred at 2 wk after immunization. Equally good incorporation of label occurred when cells were cultured with native or denatured type II collagen or type I collagen. The cellular response of nonarthritic mice immunized with denatured collagen was indistinguishable from that seen in arthritic mice. Humoral immunity was assessed by an ELISA assay for antibodies to collagen. The immunoglobulin M (IgM) response peaked at 2 wk and the IgG response at 5 wk after immunization. Antisera from arthritic mice immunized with native type II collagen were relatively specific for conformational determinants on the native type II molecule although some reactivity with denatured collagen was noted. Antisera from nonarthritic mice immunized with denatured collagen primarily recognized covalent structural determinants. It was concluded that native type II collagen was essential for the induction of arthritis and that an antibody response specific for native type II collagen may be important for the development of arthritis.

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“…42,43 Both ankles of the rats were injected with 5 Â 10 6 or 5 Â 10 5 TU of various recombinant lentiviruses or with saline on days 7 and 8. In a separate experiment, Lt.GFP and Lt.Gal1 (5 Â 10 6 TU) were injected into the left and right ankle joints of a rat with CIA on day 7, respectively, and the expression of GFP in vivo was visualized after 3 days with a Night Owl CCD camera (model LB 981, Berthold Technologies, Bad Wildbad, Germany) equipped with 480 nm excitation and 520 nm emission filters (Chroma Technology, Rockingham, VT, USA).…”

Section: Induction Of Cia and Lentivirus-mediated Gene Transfermentioning

confidence: 99%

Intra-articular lentivirus-mediated delivery of galectin-3 shRNA and galectin-1 gene ameliorates collagen-induced arthritis

et al. 2010

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Different members of the galectin family may have inhibitory or stimulatory roles in controlling immune responses and regulating inflammatory reactions in autoimmune diseases such as rheumatoid arthritis (RA). A hypothetical model of a cross talk between galectin-1 and galectin-3 has been established in the circumstance of rheumatoid joints. As galectin-3 is a positive regulator and galectin-1 is a negative regulator of inflammation and autoimmune responses, in this study we evaluated the effects of local knockdown of galectin-3 or overexpression of galectin-1 on ameliorating collagen-induced arthritis (CIA) in rats. Lentiviral vectors encoding galectin-3 small hairpin RNA (shRNA) and galectin-1, as well as two control vectors expressing luciferase shRNA and green fluorescent protein, were individually injected intra-articularly into the ankle joints of rats with CIA, and their treatment responses were monitored by measuring the clinical, radiological and histological changes. Our results show that both knockdown of galectin-3 and overexpression of galectin-1 induced higher percentages of antigen-induced T-cell death in the lymph node cells from arthritic rats. Furthermore, these treatments significantly reduced articular index scores, radiographic scores and histological scores, accompanied with decreased T-cell infiltrates and reduced microvessel density in the ankle joints. Our findings implicate galectin-3 and galectin-1 as potential therapeutic targets for the treatment of RA.

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Native type II collagen-induced arthritis in the rat. I. Incidence and humoral response to collagen.

Cited by 64 publications

References 13 publications

Incidence of serum antibodies to native type I and type II collagens in patients with inflammatory arthritis.

Incidence of serum antibodies to native type I and type II collagens in patients with inflammatory arthritis.

Nature and specificity of the immune response to collagen in type II collagen-induced arthritis in mice.

Intra-articular lentivirus-mediated delivery of galectin-3 shRNA and galectin-1 gene ameliorates collagen-induced arthritis

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