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Published on: July 22, 2011
T-suppressor cell abnormalities in type I membranoproliferative glomerulonephritis
Twelve patients with type I membranoproliferative glomerulonephritis (MPGN) have been studied. All had normal renal function, none a nephrotic syndrome, and none was on therapy. In 7/12 serum C3 and/or C4 were low. T cell subsets were analysed with OKT monoclonal antibodies and Ts function (TsF) was studied by the Concanavalin-A Enhancement test (Con-A E) and with a new assay where native OKT8+ cell function only is explored (OKT8-DEP PWM test). OKT4/OKT8 ratio was lower than controls (p less than 0.025). TsF, as studied by the Con-A E was unchanged, while OKT8-DEP PWM test showed a marked decrease (p less than 0.005). Hypocomplementaemic patients (H), as compared with normo-complementaemic patients (N), had lower OKT4/OKT8 ratio (p less than 0.01) while TsF was unchanged in both groups. These results are consistent with a functional defect of Ts activity in type I MPGN. Increased OKT8+ cells may be a compensatory response, and hypocomplementaemia may be a marker of this defect.
Twelve patients with type I membranoproliferative glomerulonephritis (MPGN) have been studied. All had normal renal function, none a nephrotic syndrome, and none was on therapy. In 7/12 serum C3 and/or C4 were low. T cell subsets were analysed with OKT monoclonal antibodies and Ts function (TsF) was studied by the Concanavalin-A Enhancement test (Con-A E) and with a new assay where native OKT8+ cell function only is explored (OKT8-DEP PWM test). OKT4/OKT8 ratio was lower than controls (p less than 0.025). TsF, as studied by the Con-A E was unchanged, while OKT8-DEP PWM test showed a marked decrease (p less than 0.005). Hypocomplementaemic patients (H), as compared with normo-complementaemic patients (N), had lower OKT4/OKT8 ratio (p less than 0.01) while TsF was unchanged in both groups. These results are consistent with a functional defect of Ts activity in type I MPGN. Increased OKT8+ cells may be a compensatory response, and hypocomplementaemia may be a marker of this defect.
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