We have attempted to verify the suggestion that synovial membrane is the result of mechanical disruption of connective tissue, and may occur at any site. Mechanical disruption of the subcutaneous connective tissue was achieved in rats and mice by the repeated injection of air. The resulting cavities developed a lining structure with many of the features of synovial membrane as judged by electron microscopy, and light microscopy using haematoxylin and eosin and van Gieson stains, esterase activity and immunofluorescent staining for Ia antigen. A structure closely resembling synovium is formed as early as 6 days, providing a convenient method for studying large quantities of facsimile synovial tissue under a wide variety of easily administered stimuli.
Normal immunological memory is thought to be underpinned by T lymphocytes. However, in rheumatoid arthritis there are indications that T‐lymphocyte control has been subverted by self‐perpetuating B lymphocytes. Potential mechanisms in other autoimmune states are less clear, but a number of observations suggest that misappropriation of immunological memory by B lymphocytes may be a common feature of human autoantibody‐associated disease. Put simply, autoantibodies drive their own production. If so, the availability of safe B‐lymphocyte‐depleting agents provides a potential means for reversal of autoimmunity.
SUMMARYWe studied the expression of hyaluronan binding proteins (HABPs) during the development of embryonic chick joints, using immunocytochemistry and biotinylated HA. The expression of actin capping proteins and of actin itself was also studied because the cytoskeleton is important in controlling HA-HABP interactions. Three cell surface HABPs were localized in the epiphyseal cartilage, articular fibrocartilage, and interzone that comprise the developing joint. Of these three HABPs, CD44 was associated with the articular fibrocartilages and interzone, whereas RHAMM and the IVd4 epitope were associated with all three tissues. Biotinylated HA was localized to interzone and articular fibrocartilages before cavity formation and within epiphyseal chondrocytes post cavitation. Actin filament bundles were observed at the developing joint line, as was the expression of the actin capping protein moesin. Manipulation of joint cavity development, using oligosaccharides of HA, disrupted joint formation and was associated with decreases in CD44 and actin filament expression as well as decreased hyaluronan synthetic capability. These results suggest that HA is actively bound by CD44 at the developing joint line and that HA-HABP interactions play a major role in the initial separation events occurring during joint formation.
TSG-6 is present within synovium and cartilage of arthritic joints, but not normal controls, and is synthesized by the resident cells. The pattern of TSG-6 expression is consistent with its proposed roles in extracellular matrix (ECM) remodeling and cellular proliferation.
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