Polymorphonuclear leucocytes and monocytes play an important role in the inflammatory response. The ability of these cell types to degranulate in response to particulate aggregated IgGl was studied after their isolation from the peripheral blood of two groups of people. These consisted of patients suffering from the chronic inflammatory disease Rheumatoid Arthritis, and, for comparison, a number of apparently healthy, normal controls. The patients' neutrophils manifest a lower responsiveness than normals in this system, while the monocytes behaved similarly in both groups. The membrane-mediated "metabolic burst" was measured directly by superoxide release and serum thiol oxidation; in neither of these was a significant difference found between normals and the patients, although patients' cells showed a trend towards a higher thiol-oxidising ability. Thus a degranulation or lysosomal defect is implicated. The effect of the addition of rheumatoid factor to the incubation medium was studied. A preparation which consisted of both IgM and IgG anti-IgG (MxRF) was found to inhibit degranulation by monocytes, while pure IgM RF had no such effect. A similar, though less marked, inhibition could alternatively be induced by adding soluble aggregates of IgGl to the degranulation-inducing system. The implications of this are discussed. The soluble aggregates and the MxRF, whilst not causing degranulation, were able to stimulate neutrophils and monocytes to release oxygen radicals. This confirms previous observations of the independence of the two reactions.
|Date of Award||1982|