We analysed the possible mechanisms responsible for the functional abnormalities reported on phagocyte cell function in IgA nephropathy patients. The oxidative metabolism by the superoxide anion ferricytochrome C reduction test on monocytes and the chemiluminescence response on neutrophils was examined in 32 patients. Moreover the expression of cell membrane structures involved in immune response and phagocytosis (i.e. Fc receptors and HLA class II antigens) was evaluated cytofluorimetrically using specific monoclonal antibodies. Our own results did not show striking differences in oxidative potential and phenotype of patients' phagocyte cells as compared with healthy controls. However a HLA class II-associated structure was found to be quantitatively more expressed in patients' monocytes than in normal controls (P less than 0.005). These findings suggest that the defective phagocyte system function reported in IgA nephropathy patients is not simply due to a loss of cell surface receptors, nor to abnormalities in intracellular metabolic pathways implying oxygen consumption. The increase in expression of some HLA class II structures, often associated with the presence of circulating IgA immune complexes, probably reflects a protracted immunological stimulation.
Phenotypic and functional analysis of circulating phagocytic cells in IgA nephropathy patients.
ROCCATELLO, Dario;FUNARO, Ada;
1989-01-01
Abstract
We analysed the possible mechanisms responsible for the functional abnormalities reported on phagocyte cell function in IgA nephropathy patients. The oxidative metabolism by the superoxide anion ferricytochrome C reduction test on monocytes and the chemiluminescence response on neutrophils was examined in 32 patients. Moreover the expression of cell membrane structures involved in immune response and phagocytosis (i.e. Fc receptors and HLA class II antigens) was evaluated cytofluorimetrically using specific monoclonal antibodies. Our own results did not show striking differences in oxidative potential and phenotype of patients' phagocyte cells as compared with healthy controls. However a HLA class II-associated structure was found to be quantitatively more expressed in patients' monocytes than in normal controls (P less than 0.005). These findings suggest that the defective phagocyte system function reported in IgA nephropathy patients is not simply due to a loss of cell surface receptors, nor to abnormalities in intracellular metabolic pathways implying oxygen consumption. The increase in expression of some HLA class II structures, often associated with the presence of circulating IgA immune complexes, probably reflects a protracted immunological stimulation.
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