OBJECTIVE: To compare the ability of normal erythrocytes and erythrocytes from systemic lupus erythematosus (SLE) patients to bind immune complexes (IC), thereby inhibiting IC deposition on polymorphonuclear leukocytes (PMN) and the consequent induction of a PMN respiratory burst (RB). METHODS: The binding of fluorescein isothiocyanate-labeled IC in 75% autologous serum to whole blood cells or isolated leukocytes from 17 SLE patients and 10 controls was assessed by flow cytometry. Reactive oxygen metabolite (ROM) production by PMN was measured as the intracellular oxidation of dihydrorhodamine 123, on stimulation with unlabeled IC. RESULTS: Erythrocyte-mediated inhibition of IC uptake by PMN reached a mean +/- SD maximum of 68 +/- 18% in controls and 29 +/- 51% in SLE patients (P < 0.05) and, in the patients, correlated inversely with disease activity. In the presence of erythrocytes from various donors, IC binding to a standard preparation of PMN and their ROM production were inversely proportional to the number of type 1 complement receptors (CR1) per donor erythrocyte. Thus, the ROM production was higher in the presence of SLE patients' erythrocytes (125 +/- 67 CR1/erythrocyte) than with erythrocytes from controls (235 +/- 118 CR1/erythrocyte). CONCLUSION: Erythrocytes from SLE patients are defective in protecting their PMN against IC deposition and induction of the RB.
OBJECTIVE: To compare the ability of normal erythrocytes and erythrocytes from systemic lupus erythematosus (SLE) patients to bind immune complexes (IC), thereby inhibiting IC deposition on polymorphonuclear leukocytes (PMN) and the consequent induction of a PMN respiratory burst (RB). METHODS: The binding of fluorescein isothiocyanate-labeled IC in 75% autologous serum to whole blood cells or isolated leukocytes from 17 SLEpatients and 10 controls was assessed by flow cytometry. Reactive oxygen metabolite (ROM) production by PMN was measured as the intracellular oxidation of dihydrorhodamine 123, on stimulation with unlabeled IC. RESULTS: Erythrocyte-mediated inhibition of IC uptake by PMN reached a mean +/- SD maximum of 68 +/- 18% in controls and 29 +/- 51% in SLEpatients (P < 0.05) and, in the patients, correlated inversely with disease activity. In the presence of erythrocytes from various donors, IC binding to a standard preparation of PMN and their ROM production were inversely proportional to the number of type 1 complement receptors (CR1) per donor erythrocyte. Thus, the ROM production was higher in the presence of SLEpatients' erythrocytes (125 +/- 67 CR1/erythrocyte) than with erythrocytes from controls (235 +/- 118 CR1/erythrocyte). CONCLUSION: Erythrocytes from SLEpatients are defective in protecting their PMN against IC deposition and induction of the RB.
Authors: I Csípö; E Kiss; P Soltész; P Antal-Szalmás; G Szegedi; J H Cohen; R P Taylor; M Kávai Journal: Clin Exp Immunol Date: 1999-12 Impact factor: 4.330
Authors: Daniel Belstrøm; Palle Holmstrup; Christian Damgaard; Tanja S Borch; Mikkel-Ole Skjødt; Klaus Bendtzen; Claus H Nielsen Journal: Infect Immun Date: 2011-01-18 Impact factor: 3.441