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  • 1
    ISSN: 1437-160X
    Keywords: Tissue architecture ; Synovial membranes ; Rheumatoid arthritis ; Ia, monocyte-macrophage antigens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Utilizing monoclonal reagents directed towards antigens of the monocyte-macrophage lineage and Ia antigens, the tissue architecture of synovial membranes obtained from patients with non-inflammatory joint diseases and patients with rheumatoid arthritis was studied. Emphasis was placed on the localization of the type I, type II and type III synoviocytes that previously had been defined by their cell surface phenotype with regard to the expression of monocyte-macrophage lineage (Mθ) and Ia antigens as well as by their phagocytic capacity or the ability to produce glycosaminoglycans. In patients with non-inflammatory joint diseases, cells with the Mθ+ Ia+ (type I) phenotype constituted the majority of synoviocytes immediately adjacent to the joint cavity; cells with this phenotype were also scattered in the subsynovial tissue and in the perivascular regions. The fibroblastoid type III cells defined by the absence of both Mθ and Ia antigens formed the major cell population in the subsynovial tissue in this patient group. In patients with rheumatoid arthritis, the Ia+ Mθ+ cells were present in a characteristic double configuration forming an intensely positive layer adjacent to the intra-articular space followed by an Ia− Mθ− layer that again was succeeded by an intensely Ia+ Mθ+ layer. Large numbers of synoviocytes bearing Mθ+ Ia+ antigens were also demonstrated in the diffusely inflamed sub-synovial tissue, in the perivascular regions as well as around and within lymphoid infiltrates. The localization of type II cells defined by the presence of Ia antigens, but the absence of Mθ antigens was indicated to be primarily in the broadened layer of synoviocytes, in the perivascular regions and within lymphoid infiltrations. While endothelial cells lacked Ia and Mθ antigens in patients with non-inflammatory joint diseases, Ia+ endothelial cells were identified in some rheumatoid samples; however, the majority of endothelial cells was also Ia negative in this patient group.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1437-160X
    Keywords: Synovial lymphocytes ; Rheumatoid arthritis ; T cell markers ; Immunoregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Analyses of the synovial tissue and fluid T lymphocytes obtained from patients with rheumatoid arthritis revealed multiple functional defects in the regulation of autologous blood B cell differentiation into cells secreting immunoglobulin. These abnormalities were not found in peripheral blood T lymphocytes from the same patients. Although the patients selected showed elevated levels of T cells expressing the T8 differentiation antigen as well as Ia antigens there was little demonstrable suppression of the blood B cell differentiation. Furthermore, the synovial T cells exhibited only minimal helper or inducer activity when tested in the same system. In contrast, patient's blood T lymphocytes gave levels of help and suppression that were not distinguishable from that of normal individuals. Co-culture experiments of blood and synovial T lymphocytes did not reveal any evidence for enhanced suppression; indeed, in most patients these cocultures resulted in marked augmentation of helper function, a phenomenon designated “helper augmentation”. These data provide evidence that rheumatoid synovial lymphocytes are characterized by marked abnormalities in immunoregulatory T cell function, including divergence of cellular activity from the immune function predicted by surface phenotype and a capacity for “helper augmentation”, a novel T cell function in man.
    Type of Medium: Electronic Resource
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