83 research outputs found
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Effect of anti-CD4 antibody treatment on inflammatory arthritis in MRL-lpr/lpr mice
MRL-lpr/lpr mice develop an inflammatory arthritis in association with other manifestations of autoimmunity. Although a variety of immune cell disturbances have been described in these mice, the relationship of these abnormalities to the pathogenesis of arthritis has not yet been determined; the role of T cells is especially unclear since synovial hypertrophy and joint erosions have been noted in some studies in the absence of a significant T cell infiltrate. Therefore, to determine if T cells are required for arthritis in MRL-lpr/lpr mice, we evaluated the effects of prolonged treatment with a monoclonal anti-CD4 antibody. Knee joints from treated mice had markedly reduced arthritis compared to saline-treated control animals as measured by the degree of synovial hypertrophy and inflammation. Nephritis in these mice was concomitantly reduced. In contrast, rheumatoid factor levels were not affected by CD4+ cell depletion, despite significant effects on anti-DNA. These results indicate that in MRL-lpr/lpr mice anti-CD4 therapy can inhibit arthritis, suggesting an important role of T cells in the pathogenesis of this lesion
Effect of commercial immunoglobulin G preparation on human monocyte Fc-receptor dependent binding of antibody coated platelets
This study examined the in vitro effect of a commercial immunoglobulin preparation on human monocytes and the Fc-receptor dependent binding of antibody coated platelets. Monocytes were exposed to Sandoglobulin in vitro and subsequently examined for membrane surface bound IgG. Dramatic increments of surface IgG were found which were maximal with 18 h exposure and somewhat higher at 4°C than 37°C. Ultracentrifugations of Sandoglobulin immediately prior to monocyte exposure reduced the monocyte membrane IgG by 75%. The 18 h exposure at 37°C produced dramatic impairment of monocyte Fc-receptor binding of IgG coated platelets (P \u3c 0.001) while exposure for 18 h at 4°C produced a modest impairment of Fc-receptor function. These studies indicate that Sandoglobulin contains IgG aggregates which are able to firmly bind to the monocyte surface in a time and temperature dependent fashion. The dramatic impairment of Fc-receptor function at 37°C and not at 4°C suggests that Fc-receptor modulation, as well as competitive inhibition/steric hindrance, contribute to impairment of monocyte Fc-receptor function
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