Surface Ultrastructure of Rheumatoid Articular Cartilage

Kimura, Hiroshi; Tateishi, Hiroki; Ziff, Morris

doi:10.1002/art.1780200508

Cited by 44 publications

(10 citation statements)

References 34 publications

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“…Histologic analysis of joint damage in RA has resulted in the report of a similar observation (38). In addition, in humans, surface damage can be seen microscopically in areas that are macroscopically normal (39). We also noted this latter result with regard to the lack of observable gross pathology indicative of chronic immune synovitis, after intravenous administration of antiproteoglycan monoclonal antibodies.…”

Section: Discussionsupporting

confidence: 59%

Evidence that a humoral immune response to autologous cartilage proteoglycan can participate in the induction of cartilage pathology

Kresina

Yoo

Goldberg

1988

Arthritis & Rheumatism

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We examined antiproteoglycan antibodies as an autoimmune response for induction of synovitis. This hypothesis was studied by monitoring humoral antiproteoglycan antibody following IgG induction of experimental immune synovitis, localization in the articular cartilage of an autologous immune response, and loss of proteoglycan from cartilage following intravenous administration of antiproteoglycan monoclonal antibodies. The data support the hypothesis that autoimmunity to cartilage macromolecules may play a role in the etiopathogenesis of arthritis.Experimental antigen-induced immune synovitis has been widely used as a model of rheumatoid arthritis (RA) in the study of the pathophysiology of the human disease. Salient features of the experimental model of synovitis and RA include deposition of immune complexes and complement in joint cartilage (1,2), hyperplasia of the synovium (3,4), antibody deposition in affected synovia (5,6), cell-mediated and humoral immune responses to the genetically distinct interstitial collagens (7,8), pannus formation, cartilage erosion, and ligament destruction (3,4,7,9).Experimental antigen-induced arthritis has been described in rabbits immunized to homologous or heterologous fibrin (3), and in immunized rabbits receiving intraarticular injection of egg albumin (lo), bovine serum albumin (BSA) (lo), cartilage proteoglycan subunits (1 l), and immunoglobulin (9). Studies characterizing antibody synthesis in these models have noted a localization of antibody specific for the arthritis, initiating immunogens in the synovium (1 3).A pathophysiologic role for proteoglycan molecules in the inflammation and erosion of cartilage matrix that is observed in chronic synovitis was suggested by the observation of high concentrations of cartilage wear particles in human synovial fluids aspirated from arthritic joints (12). Recently, studies using radioimmunoassays have measured fragments of proteoglycan moieties in the synovial fluid and serum of patients with RA (13). Further studies using animal models of arthritis have implicated autoimmunity to proteoglycan molecules in the pathophysiology of synovitis. Champion and coworkers (14,15) noted cellmediated and humoral immune responses to cartilage proteoglycan in rabbits with experimentally induced synovitis. Van Eden et a1 (16) have reported that the induction of adjuvant arthritis in rats is characterized through the generation of a T lymphocyte clone that recognizes proteoglycan molecules. Mikecz et a1 (17) have recently reported that immunization of inbred strains of mice with cartilage proteoglycan can induce an inflammation of the joint which resembles, in some aspects, rheumatoid arthritis and ankylosing spondylitis.In recent studies from this laboratory, the antiproteoglycan immune response observed in chronic

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Section: Discussionsupporting

confidence: 59%

Evidence that a humoral immune response to autologous cartilage proteoglycan can participate in the induction of cartilage pathology

Kresina

Yoo

Goldberg

1988

Arthritis & Rheumatism

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“…While large numbers of PMN are present in rheumatoid synovial fluid, it is generally agreed that PMN are not present in significant numbers on the pannus-free surface of cartilage (10) or in the rheumatoid pannus itself (13). However, it has recently been reported that large numbers of PMN are present at the pannus-cartilage junction (14) and also that some PMN are present on the surface of rheumatoid cartilage (1 1); this suggests that these cells may participate in rheumatoid cartilage destruction.…”

Section: Discussionmentioning

confidence: 99%

Interaction of polymorphonuclear leukocytes with immune complexes trapped in rheumatoid articular cartilage

Ugai

Ishikawa

Hirohata

et al. 1983

Arthritis & Rheumatism

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When rheumatoid articular cartilage samples were incubated with normal polymorphonuclear leukocytes (PMN) in vitro, large numbers of PMN were seen attached to the articular surface. As observed by electron microscopy, significant numbers of these cells invaded the cartilage tissue and phagocytosed amorphous material which presumably contained immune complexes. In control cartilage from osteoarthritic, pyogenic, and normal subjects, only a few PMN were attached to the articular surface after incubation with PMN. These results demonstrate that immune complexes trapped in the superficial region of the rheumatoid articular cartilage may play an important role in the destruction of cartilage by the release of lysosomal enzymes from PMN.

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“…The evidence for this is based on the presence of humoral and cellular immunity to these elements in patients as well as their arthritogenic potenlial in animal models of arthritis [1][2][3], Chondrocytes produce and maintain cartilage matrix and whilst humoral [4] and cellular [5] re.sponses to chondrocytes have been reported in both osteoarthritis (OA) and rheumatoid arthritis (RA), their role in these conditions is not clear. Ultrastructural studies of rheumatoid articular eartilage have demonstrated cartilage degradation in areas free of pannus tissue [6] and immunohistochemical studies of the cartilage pannus junction in RA suggest that some ofthe fibroblast-like cells identified in this important region may be of ehondrocytc origin [7,8], Other studies ofthis region have shown MHC class II bearing cells whieh also demonstrate intracellular CIL a cartilage specific collagen [9]. The nature of these eells is unknown but il is speculated that they are phagocytes flO].…”

Section: Introductionmentioning

confidence: 99%

Cellular responses to human chondrocytes: absence of allogeneic responses in the presence of HLA-DR and ICAM-1

Jobanputra

Corrigall

Kingsley

et al. 1992

Clinical and Experimental Immunology

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SUMMARYTo assess the accessory cell funcuon of human articular chondrocytes. we assessed the ability of hunian chondrocytes lo stimuliite allogeneic peripheral biood mononuclear cells (PBMC) and to support phyiohacmagglutinin (PHA)-induccd proliferation of highly purified T ceils. We also examined the surface expression of HLA-DR and ICAM-1 on the chondrocytes both unstimulated and stimulated with cytokines//jnVre;. Chondrocytesfailed to stimulate allogeneic PBMC despite the constitutive expression of MHC class I molecules and the cytokine-induced expression of class II molecules but were able lo support Tccll proliferation to PHA. IFN-v and ^od limited extent, IL-l/f. induced class 11 expression on chondrocytes. ICAM-1 was present on 94-99".. of freshly isolated ceils; this declined with culture (17-59%; P

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Surface Ultrastructure of Rheumatoid Articular Cartilage

Cited by 44 publications

References 34 publications

Evidence that a humoral immune response to autologous cartilage proteoglycan can participate in the induction of cartilage pathology

Evidence that a humoral immune response to autologous cartilage proteoglycan can participate in the induction of cartilage pathology

Interaction of polymorphonuclear leukocytes with immune complexes trapped in rheumatoid articular cartilage

Cellular responses to human chondrocytes: absence of allogeneic responses in the presence of HLA-DR and ICAM-1

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