Effects of Rheumatoid Factor and Complement on Soluble Immunoglobulin G Complexes: 51CrCI3 Labeling and Precipitation Studies

This study examines aggregate-cell interacations in a newly applied neutrophil monolayer system, as an in vitro model of rheumatoid inflammation. Insoluble and soluble immunoglobulin G (IgG) aggregates were combined with rheumatoid factor (RF) to produce IgG-RF complexes. The presence of RF did not significantly change the uptake of the insoluble aggregates by neutrophils as measured in the monolayer system. Neutrophils exposed to these aggregates showed significantly (P less than 0.005) greater uptake than those exposed to soluble aggregates, and the presence or absence of serum did not change these results. Increasing concentrations of radiolabeled aggregates to 1.5 mg/ml and cells to 5 X 10(6) neutrophils/ml increased cell-associated radioactivity. Addition of cytochalasin B to 5 mg/ml progressively depressed cell-associated radioactivity. Gold, but not aspirin, in therapeutic concentrations seemed to suppress aggregate uptake. This system offers a method for quantitatively assaying aggregate uptake which may be an important component of the rheumatoid inflammatory process.

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Neutrophil migration in response to chemotactic factors

Turner

Johnson

Mountz

et al. 1983

Inflammation

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The effects of various chemotactic factor generation conditions and several chemotherapeutic agents on neutrophil migration were determined using in vitro assay systems designed as models for inflammatory processes occurring in the synovial cavities of patients with rheumatoid arthritis. The microtubule-promoting agent concanavalin A and the microfilament-disrupting agent cytochalasin B were shown in these systems to inhibit neutrophil migration towards zymosan-activated serum-derived chemotactic factors. Neutrophils, immunoglobulin G aggregates, and serum were required for maximum generation of comparable chemotactic factors. Insoluble immunoglobulin G aggregates with or without rheumatoid factor produced more chemotactic factor activity on interaction with neutrophils than soluble immunoglobulin G aggregates. Exposure of neutrophils to supratherapeutic levels of the nonsteroidal antiinflammatory agent aspirin decreased neutrophil response to chemotactic factors while exposure to the slow-acting or immunomodulating agents gold, D-penicillamine, or azathioprine had no effect on this neutrophil function. In vitro systems employing neutrophils, insoluble aggregates, and serum may offer useful means for assaying drug effects on important functional components of the rheumatoid inflammatory process.

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Effects of Rheumatoid Factor and Complement on Soluble Immunoglobulin G Complexes: 51CrCI3 Labeling and Precipitation Studies

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Drug and rheumatoid factor effects on the uptake of immunoglobulin g aggregates by neutrophil monolayers

Neutrophil migration in response to chemotactic factors

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