Electron microscopic observations on the rheumatoid synovial membrane

Norton, Walter L.; Ziff, Morris

doi:10.1002/art.1780090405

Cited by 116 publications

(39 citation statements)

References 15 publications

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“…Strongly DR+ lining cells were identified as the type A, or macrophage-type, cells described by Barland et a1 (28), and largely DR-cells were identified as the type B, or fibroblast-type, cells. Intermediately staining DR+ cells of a type previously described as type I1 (37) or type C cells (38,39) were also observed.…”

Section: Discussionmentioning

confidence: 67%

Electron microscopic study of HLA‐DR and monocyte/macrophage staining cells in the rheumatoid synovial membrane

Iguchi

Kurosaka

Ziff

1986

Arthritis & Rheumatism

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We examined synovial membrane samples from 6 rheumatoid arthritis (RA) and 3 osteoarthritis patients and from 1 normal subject, by an immunoelectron microscopic technique using anti-HLA-DR (anti-Ia) and anti-monocyte/macrophage (63D3) monoclonal antibodies. In the lining layer, the type A macrophage-like cells were strongly DR+ and 63D3+, whereas the type B fibroblast-like cells were almost completely negative. Lymphocyte-rich areas (containing more than 90% densely packed lymphocytes) showed weak and patchy DR staining of the lymphocytes. In these areas, 3 4 % of the cells were macrophage-like cells which were 63D3-, a type of staining compatible with that of the interdigitating cell (IDC). In the plasma cell-containing (transitional) areas, many strongly DR+ macrophage-like cells were observed in close contact with lymphocytes and plasma cells. Ten to twenty percent of these cells were 63D3-, which suggests that they were IDC. Cells with the structural appearance of IDC were most frequently seen in those transitional areas which contained elevated concentrations (50-70%) of lymphocytes. In uninfiltratFrom the Harold C.

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Section: Discussionmentioning

confidence: 67%

Electron microscopic study of HLA‐DR and monocyte/macrophage staining cells in the rheumatoid synovial membrane

Iguchi

Kurosaka

Ziff

1986

Arthritis & Rheumatism

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“…T h e contribution of cellular immunity in this chronic synovitis is not known. I t is well established that plasma cells are present (1) and that immunoglobulins are actively pro- duced and secreted (2). However electron microscopic studies showing extensive blast cell formation (3) and an inhibitor of macrophage migration in supernatants of cultures of rheumatoid synovial tissue (4) point to the participation of cellular immunity in the local manifestations of rheumatoid disease.…”

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confidence: 99%

Experimental arthritis produced by injection of mediators of delayed hypersensitivity

Andreis

Šťastný

Ziff

1974

Arthritis & Rheumatism

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Arthritis was produced in the rabbit by intraarticular injection of a preparation of mediators of cellular immunity (lymphokines) obtained from KLH-sensitized lymphocytes. Following three injections, a chronic synovitis developed characterized by synovial effusion, hyperplasia of the lining layer and infiltration of the sublining layer with histiocytes and fibroblasts. These findings indicate that mediators of cellular immunity may produce a chronic synovitis when injected into the normal joint. They also demonstrate a mechanism whereby the cellular immune response may produce synovial inflammation.It is generally accepted that an active immunologic reaction involving the synovial membrane plays a major role in the pathogenesis of rheumatoid arthritis. T h e contribution of cellular immunity in this chronic synovitis is not known. I t is well established that plasma cells are present (1) and that immunoglobulins are actively pro- Submitted for publication September 25, 1973; Accepted April 8, 1974. of lymphocytes from immune animals or patients with specific antigen leads to the release of these substances whose biologic

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“…In rheumatoid arthritis, synovial fluid has been shown to contain raised levels of bradykinin (Melmon et al, 1967;Keele & Eisen, 1970) and prostaglandin (Higgs et al, 1974). Mast cells are plentiful in the rheumatoid synovium (Norton & Ziff, 1966) and histamine and histidine-decarboxylase activity have been detected in the rheumatoid synovial membrane (Roth, Polley & Code, 1964).…”

Section: Discussionmentioning

confidence: 99%

THE EFFECTS OF PROSTAGLANDIN E₁, BRADYKININ AND HISTAMINE ON CANINE SYNOVIAL VASCULAR PERMEABILITY

Grennan

Mitchel

Miller³

et al. 1977

British J Pharmacology

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I The relative effects of prostaglandin E1, bradykinin and histamine on canine synovial vascular permeability were investigated by a method based on the measurement of the amounts of radiolabelled dextran (molecular weight 20,000) leaking from the circulation into the synovial cavity.2 Bradykinin, prostaglandin E1 and histamine in that order of potency all increased synovial vascular permeability. Threshold concentrations were 0.3 JiM, 3 jiM and 30 JIM respectively. 3 The effects of infusion of prostaglandin E1 combined with either bradykinin or histamine were greater than mere summation.

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Electron microscopic observations on the rheumatoid synovial membrane

Cited by 116 publications

References 15 publications

Electron microscopic study of HLA‐DR and monocyte/macrophage staining cells in the rheumatoid synovial membrane

Electron microscopic study of HLA‐DR and monocyte/macrophage staining cells in the rheumatoid synovial membrane

Experimental arthritis produced by injection of mediators of delayed hypersensitivity

THE EFFECTS OF PROSTAGLANDIN E₁, BRADYKININ AND HISTAMINE ON CANINE SYNOVIAL VASCULAR PERMEABILITY

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Electron microscopic observations on the rheumatoid synovial membrane

Cited by 116 publications

References 15 publications

Electron microscopic study of HLA‐DR and monocyte/macrophage staining cells in the rheumatoid synovial membrane

Electron microscopic study of HLA‐DR and monocyte/macrophage staining cells in the rheumatoid synovial membrane

Experimental arthritis produced by injection of mediators of delayed hypersensitivity

THE EFFECTS OF PROSTAGLANDIN E1, BRADYKININ AND HISTAMINE ON CANINE SYNOVIAL VASCULAR PERMEABILITY

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THE EFFECTS OF PROSTAGLANDIN E₁, BRADYKININ AND HISTAMINE ON CANINE SYNOVIAL VASCULAR PERMEABILITY