Autoantibodies to type II collagen: occurrence in rheumatoid arthritis, other arthritides, autoimmune connective tissue diseases, and chronic inflammatory syndromes.

Choi, Edward K. K.; Gatenby, Paul A.; McGill, Neil; Bateman, John F.; Cole, William G.; York, John R.

doi:10.1136/ard.47.4.313

Cited by 76 publications

(40 citation statements)

References 13 publications

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“…Thus, both autoreactive T and B cells specific for CII escape deletion in RA, and these are apparently not properly regulated. It is not clear how immunological tolerance to CII is broken and whether this breakage of self tolerance represents an early disease-driving event or an epiphenomenon of late-stage disease [11,12,13]. In this respect our present data provide first evidence that already at very early stages of RA, CII is targeted by autoantibody responses.…”

Section: Discussionmentioning

confidence: 68%

“…On the other hand, much more is known about the potential of autoantibodies directed toward collagen type II (CII) epitopes, which are recognized in cartilage-specific autoimmune responses in RA patients, to induce an erosive arthritis in naive mice upon antibody transfer [9,10]. However, anti-CII autoantibodies are detectable in the circulation in only 5-15% of RA patients, and divergent data has been published on the issue of whether CII autoimmunity represents an early or late event in the disease course [11,12]. In the present investigation, we tested the hypothesis of whether CII might be a substrate for structural modification by PAD enzymes, which could result in a breakage of self tolerance to this cartilagespecific autoantigen.…”

Section: Introductionmentioning

confidence: 99%

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Humoral immune response to citrullinated collagen type II determinants in early rheumatoid arthritis

et al. 2005

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Collagen type II (CII) is a relevant joint‐specific autoantigen in the pathogenesis of rheumatoid arthritis (RA). Whereas the reasons for the breakage of self tolerance to this major cartilage component are still enigmatic, T cell responses to glycosylated CII determinants in RA patients indicate that post‐translational modifications play a role. Since the conversion of arginine into citrulline by peptidylarginine deiminases (PAD) in some non‐joint‐specific antigens such as filaggrin or fibrin has been shown to give rise to RA‐specific humoral immune responses, we investigated whether PAD modification of cartilage‐specific CII might affect its recognition by circulating autoantibodies in early RA. In vitro treatment with purified PAD led to arginine deimination of native CII or of synthetic CII peptides as evidenced by amino acid analysis. The citrullination resulted in modified recognition of the immunodominant CII epitope C1III (amino acid residues 359–369) by murine and human antibodies. In a cohort of early RA patients (n=286), IgG antibodies directed toward a synthetic citrullinated C1III peptide (citC1III‐P) were detectable with a prevalence of 40.4%. The partial autoantibody cross‐reactivity between citC1III‐P and citrullinated peptides mimicking epitopes of the cytoskeletal autoantigen filaggrin suggests that autoimmunity to cartilage‐specific modified self might be a critical intermediate bridging recognition of PAD‐modified extra‐articular autoantigens with the disruption of tolerance to native cartilage constituents.

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Section: Discussionmentioning

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Humoral immune response to citrullinated collagen type II determinants in early rheumatoid arthritis

et al. 2005

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“…Serum antibodies to cartilage collagen and chondrocyte membrane proteins have been detected in joint disease (Niebauer et al 1987, Mollenhauer et al 1988, Paroczai and Nemeth-Csbka 1988, Choi et al 1988). …”

Section: Markersmentioning

confidence: 99%

Markers of cartilage metabolism in arthrosis

Lohmander

1991

Acta Orthopaedica Scandinavica

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“…There is evidence for the presence of autoantibodies against proteoglycans and collagens, especially type I1 collagen (5)(6)(7)(8)(9). Parallel studies investigating cell-mediated immune response have documented a T cell responsiveness to these connective tissue elements; however, this response was usually not very vigorous (10)(11)(12)(13) The results obtained in the present investigation demonstrate that there is a striking reactivity against chondrocyte membranes in patients with RA and an unexpected response to both chondrocyte and fibroblast cell membranes in patients with OA; thereby distinguishing these 2 patient groups.…”

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confidence: 99%

Cellular immune response toward human articular chondrocytes. T cell reactivities against chondrocyte and fibroblast membranes in destructive joint diseases

Alsalameh¹,

Mollenhauer²,

Hain³

et al. 1990

Arthritis & Rheumatism

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Articular cartilage is one of the major targets in destructive joint diseases in humans. We studied cellular immune reactions against cartilage cell‐surface membranes, because it has recently been suggested that these represent possible antigenic structures, based upon the observation of autoantibodies with this specificity in certain joint diseases. A striking T cell reactivity toward chondrocyte membranes was found both in blood and synovial tissue from patients with rheumatoid arthritis. This reactivity was strongly dependent on the presence of monocytes and had all the characteristics of an antigen‐driven process. Clonal analysis demonstrated high precursor frequencies in peripheral blood T cells that were reactive against chondrocyte membranes. This response to chondrocyte membranes greatly exceeded the T cell stimulation induced by membranes from other sources such as fibroblasts or epithelial cells. In contrast to patients with rheumatoid arthritis, individuals with osteoarthritis showed a strong peripheral blood and synovial fluid T cell response not only to chondrocyte membranes, but also to fibroblast membrane material. However, there was no reactivity to epithelial cell membranes. Normal donors generally did not show significant responses to any membrane preparation. These data indicate that there is a strong T cell reactivity toward chondrocyte membranes in destructive joint disorders, and this may significantly contribute to the pathogenetic processes that occur in these diseases.

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Autoantibodies to type II collagen: occurrence in rheumatoid arthritis, other arthritides, autoimmune connective tissue diseases, and chronic inflammatory syndromes.

Cited by 76 publications

References 13 publications

Humoral immune response to citrullinated collagen type II determinants in early rheumatoid arthritis

Humoral immune response to citrullinated collagen type II determinants in early rheumatoid arthritis

Markers of cartilage metabolism in arthrosis

Cellular immune response toward human articular chondrocytes. T cell reactivities against chondrocyte and fibroblast membranes in destructive joint diseases

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