Demonstration of anticollagen antibodies in rheumatoid arthritis synovial fluids by <sup>14</sup>c‐radioimmunoassay

Menzel, J; Steffen, C; Kolarz, G; Kojer, Marina; Smolen, Josef S.

doi:10.1002/art.1780210212

Cited by 55 publications

(26 citation statements)

References 13 publications

(7 reference statements)

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“…These antibodies engage in the formation of complement-binding antigen-antibody complexes which are said to play a major part in the induction and perpetuation of synovial inflammation. In the SF of human patients with RA and OA, anticollagen antibodies (Menzel et al, 1976(Menzel et al, , 1978Stuart et al, 1983;Jasin, 1985) and immune complexes (Cooke, 1980) have been discovered. In RA, these antibodies are produced locally by plasma cells that are located in the synovial tissue (Smiley et al, 1968).…”

Section: Humoral Immunity In Cruciate Diseasementioning

confidence: 99%

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

Doom

Bruin

Rooster

et al. 2008

Veterinary Immunology and Immunopathology

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The majority of studies on cranial cruciate ligament (CrCL) disease to date have been carried out on dogs that already sustained a CrCL rupture, which is the end-stage of the disease. Investigations have recently been carried out to study humoral and cellular immunopathological mechanisms in predisposed dogs before clinical rupture of the contralateral CrCL. The cruciate ligaments are mainly composed of collagen type I, and immune responses to collagen have been suggested as a cause of CrCL degradation in dogs. None of these investigations showed evidence that anticollagen type I antibodies alone initiate CrCL damage. However, in predisposed dogs a distinct anticollagen type I antibody gradient was found towards the contralateral stifle joint that eventually sustained a CrCL rupture, suggesting that there was an inflammatory process present in these joints before detectable joint instability occurred. The importance of cellular reactivity to collagen type I in cruciate disease also remains unclear. Peripheral blood mononuclear cell proliferation to collagen type I was very diverse in dogs with cruciate disease whereas some sham operated dogs and healthy dogs tested positive as well. It is not yet determined whether cellular reactivity to collagen type I exists locally in the stifle joints nor whether this could initiate CrCL degradation.Inflammatory processes within the stifle joint can alter the composition of the cruciate ligaments. In animal models of immunemediated synovitis, the mechanical strength of the CrCL is significantly reduced. Immunohistochemical studies on synovial tissues from dogs with rheumatoid arthritis and dogs with cruciate disease revealed that the pathologic features are similar in both joint pathologies and that the differences are mainly quantitative. Joint inflammation induced by biochemical factors such as cytokines has been implied in CrCL degeneration. In several studies, the levels of pro-inflammatory and T helper cytokines were measured in dogs that sustained a CrCL rupture, but the exact role of the various cytokines in the pathogenesis of CrCL disease remains inconclusive. More recently, the levels of the cytokines have been investigated over time in predisposed dogs before and after CrCL rupture. IL-8 expression tended to be higher in stifle joints that will rupture their CrCL during the next 6 months than in those that will not, indicating an inflammatory process in these joints before clinical rupture.

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Section: Humoral Immunity In Cruciate Diseasementioning

confidence: 99%

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

Doom

Bruin

Rooster

et al. 2008

Veterinary Immunology and Immunopathology

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“…These antibodies have been demonstrated to react to some degree with all types of collagen tested (9), but major interest has centered on type I collagen, which is found predominantly in skin, bone, vessels, and at joint surfaces, and type I1 collagen, which is found in hyaline cartilage. Antibodies have been shown to react with native collagens (M), denatured collagens (2), or both native and denatured collagens (3,8,9,11).…”

Section: Discussionmentioning

confidence: 99%

“…However, with the ' introduction of radioimmunoassays to detect collagen antibodies, reactivity has been detected in almost all sera tested, from patients and controls (4,8,9,11). The significance of this reactivity has not been certain.…”

Section: Discussionmentioning

confidence: 99%

Collagen antibodies in rheumatoid arthritis. SIgnificance of antibodies to denatured collagen and their association with HLA‐DR4

Rowley

Tait

Mackay

et al. 1986

Arthritis & Rheumatism

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The frequency, specificity, and HLA associations of antibodies to collagen were examined in 54 patients with severe rheumatoid arthritis (RA) and in 67 control subjects, using native and denatured bovine type I1 collagen as reactants in a solid-phase radioimmunoassay. Reactivity to denatured collagen was significantly higher in the RA patients than in the controls (P = 0.0041). Reactivity to native collagen was substantially lower than reactivity to denatured collagen and was simikar in RA patients and controls. DR4 positive RA patielnts had significantly greater reactivity to denatured collagen compared with DR4 negative RA patients (P = 0.03), but levels of antibody to native collagen were similar among DR4 positive and DR4 negative patients. These data lend support to the idea that denatured collagen is an important secondary reactant in immunemediated perpetuation of RA.Studies conducted during the past several years have demonstrated the presence of antibodies to collagen in the serum (1-9) and synovial fluid (9-1 1) of patients with rheumatoid arthritis (RA), although it has not been possible to relate the presence or titer of collagen antibody to the course or severity of the disease. These studies have used a variety of collagen types as antigen, and often no distinction has been made between antibodies to native collagen and antibodies to denatured collagen. For this reason, we sought to reexamine the presence of antibodies to type I1 collagen in patients with RA, with particular attention to reactivity with native collagen versus denatured type 11 collagen. We developed a solid-phase radioimmunoassay using either native or denatured bovine type I1 collagen as antigen, and using staphylococcal protein A as the radioactively labeled marker to detect IgG antibodies. Protein A binds to IgG in human serum (although not to IgG3, which is 1-3% of total human IgG), and binds only slightly to IgM (12). IgG antibodies were chosen for study because of the good correlation between levels of IgG and IgM antibodies to native collagen in rheumatoid arthritis, demonstrated by Clague et a1 (6).Since normal human serum contains apparent anticollagen reactivity (1,4,7,8), we determined whether the serum reactivity in patients with RA differed qualitatively and/or quantitatively from that in normal subjects. Also, since HLA-DR4 is a major risk factor for RA (13), we correlated the presence of HLA-DR4 and associated haplotypes with levels of antibody to denatured and native type I1 collagen.

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“…Moreover, fibrosis of the liver leads to he patocellular injury, which by itself engen ders inflammation, and chronic inflammation may cause connective tissue destruction [18]. Thus disorders other than liver disease cha racterized by chronic inflammation were shown to be associated with the appearance of ACA: rheumatoid arthritis [19,20], thromboangiitis [21] and relapsing poly chondritis [22], Only in rheumatoid arthritis the antibody class of the ACA has been determined and was shown to consist of IgG [20], which was confirmed in our laboratory (unpublished observation).…”

Section: Discussionmentioning

confidence: 99%

Autoantibodies to Collagen in Patients with Chronic Liver Diseases

Menzel¹,

Smolen²,

Renner³

et al. 1980

Int Arch Allergy Immunol

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Sera of patients with various liver diseases were investigated for the presence of autoantibodies to type I collagen with a sensitive radioimmunoassay employing ³H-labelled collagen type I. A high percentage (69%) of patients with chronic liver diseases, equally distributed between chronic active hepatitis and alcoholic liver disease, was found to possess antibodies to denaturated type I collagen, while no antibodies against native collagen were found. These antibodies belonged predominantly to the IgA immunoglobulin class. None of the patients with acute hepatitis or cholestatic liver disease, nor the healthy individuals investigated had IgA-anticollagen antibodies. These findings may be useful as a parameter for the detection of chronic liver disease.

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Demonstration of anticollagen antibodies in rheumatoid arthritis synovial fluids by ¹⁴c‐radioimmunoassay

Cited by 55 publications

References 13 publications

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

Collagen antibodies in rheumatoid arthritis. SIgnificance of antibodies to denatured collagen and their association with HLA‐DR4

Autoantibodies to Collagen in Patients with Chronic Liver Diseases

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Demonstration of anticollagen antibodies in rheumatoid arthritis synovial fluids by 14c‐radioimmunoassay

Cited by 55 publications

References 13 publications

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

Collagen antibodies in rheumatoid arthritis. SIgnificance of antibodies to denatured collagen and their association with HLA‐DR4

Autoantibodies to Collagen in Patients with Chronic Liver Diseases

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Demonstration of anticollagen antibodies in rheumatoid arthritis synovial fluids by ¹⁴c‐radioimmunoassay