Diminished ability of erythrocytes from patients with systemic lupus erythematosus to limit opsonized immune complex deposition on leukocytes and activation of granulocytes

C H Nielsen, J M Rasmussen, A Voss, P Junker, R G Leslie

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

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.

OriginalsprogEngelsk
TidsskriftArthritis & Rheumatism
Vol/bind41
Udgave nummer4
Sider (fra-til)613-22
Antal sider10
ISSN0004-3591
DOI
StatusUdgivet - apr. 1998

Fingeraftryk

Neutrophils
Respiratory Burst
Oxygen
Complement Receptors
Fluorescein
Flow Cytometry
Serum

Citer dette

@article{fc759f6c4a954c1c848f96360441f149,
title = "Diminished ability of erythrocytes from patients with systemic lupus erythematosus to limit opsonized immune complex deposition on leukocytes and activation of granulocytes",
abstract = "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.",
keywords = "Adolescent, Adult, Antigen-Antibody Complex, Buffers, Erythrocytes, Female, Granulocytes, Humans, Kinetics, Leukocytes, Lupus Erythematosus, Systemic, Male, Middle Aged, Monocytes, Neutrophil Activation, Opsonin Proteins, Phycoerythrin, Protein Binding, Receptors, Complement, Respiratory Burst, Journal Article, Research Support, Non-U.S. Gov't",
author = "Nielsen, {C H} and Rasmussen, {J M} and A Voss and P Junker and Leslie, {R G}",
year = "1998",
month = "4",
doi = "10.1002/1529-0131(199804)41:4<613::AID-ART8>3.0.CO;2-A",
language = "English",
volume = "41",
pages = "613--22",
journal = "Arthritis & Rheumatology",
issn = "2326-5205",
publisher = "Heinemann",
number = "4",

}

Diminished ability of erythrocytes from patients with systemic lupus erythematosus to limit opsonized immune complex deposition on leukocytes and activation of granulocytes. / Nielsen, C H; Rasmussen, J M; Voss, A; Junker, P; Leslie, R G.

I: Arthritis & Rheumatism, Bind 41, Nr. 4, 04.1998, s. 613-22.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Diminished ability of erythrocytes from patients with systemic lupus erythematosus to limit opsonized immune complex deposition on leukocytes and activation of granulocytes

AU - Nielsen, C H

AU - Rasmussen, J M

AU - Voss, A

AU - Junker, P

AU - Leslie, R G

PY - 1998/4

Y1 - 1998/4

N2 - 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.

AB - 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.

KW - Adolescent

KW - Adult

KW - Antigen-Antibody Complex

KW - Buffers

KW - Erythrocytes

KW - Female

KW - Granulocytes

KW - Humans

KW - Kinetics

KW - Leukocytes

KW - Lupus Erythematosus, Systemic

KW - Male

KW - Middle Aged

KW - Monocytes

KW - Neutrophil Activation

KW - Opsonin Proteins

KW - Phycoerythrin

KW - Protein Binding

KW - Receptors, Complement

KW - Respiratory Burst

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1002/1529-0131(199804)41:4<613::AID-ART8>3.0.CO;2-A

DO - 10.1002/1529-0131(199804)41:4<613::AID-ART8>3.0.CO;2-A

M3 - Journal article

VL - 41

SP - 613

EP - 622

JO - Arthritis & Rheumatology

JF - Arthritis & Rheumatology

SN - 2326-5205

IS - 4

ER -