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Immune complex binding to erythrocyte‐CR1 (CD 35), CR1 expression and levels of erythrocyte‐fixed C3 fragments in SLE outpatients
Author(s) -
Jepsen HANS HENRIK,
Rasmussen JENS MØLLER,
Teisner BØRGE,
SchrØDer LISE,
Holmskov UFFE,
JarlbæK LENE,
Isager HENRIK,
Svehag SVENERIK
Publication year - 1990
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1990.tb04981.x
Subject(s) - antigen , immune system , medicine , lupus erythematosus , immunology , endocrinology , immune complex , anti dsdna antibodies , mixed connective tissue disease , ic3b , epitope , microbiology and biotechnology , chemistry , antibody , complement system , biology
Erythrocytes (E) from a cross‐sectional group of 22 outpatients with systemic lupus erythematosus (SLE) and/or mixed connective tissue disease (MCTD), the majority without active disease (n = 14), were analyzed for CR1 antigen expression and capacity to bind complement opsonized, radiolabeled immune complexes (IC). Furthermore, E‐bound C3 fragments and the plasma C3d concentration were determined. E‐bound C3b/iC3b fragments were not elevated in patients with SLE, whereas E from 11 out of 22 SLE patients had increased C3d levels which correlated with the plasma C3d concentration (R s 0.73, p < 0.001). E‐fixed C3d fragments did not affect the binding of Mab or preopsonized IC to E‐CR1 and were not correlated with disease activity or medical treatment. Antigen expression of E‐CR1 measured by ELISA or agglutination showed positive correlation with the IC binding capacity of E‐CR1 (R s 0.92 and 0.72 respectively, p < 001). The IC binding capacity of E‐CR1 from SLE patients was significantly reduced (p > 0.005), whereas the antigen expression of CR1 (ELISA) on E from the patients did not differ from that of E from healthy donors (p > 0.1). E‐CR1 antigen was measured by Mab reacting with an epitope outside the IC‐binding site of E‐CR1. E‐CR1 antigen expression or IC binding showed no correlation either with disease activity or prednisolone treatment. However, 4 og 5 patients with MCTD and 4 of 5 patients receiving Imurel® were found to have low E‐CR1 expression and capacity to bind IC. Thus, measurement of antigenic E‐CR1 in a cross‐sectional group of SLE outpatients by use of Mab reacting with an epitope outside the ligand‐binding region of CR1 did not reveal a significantly reduced CR1 expression. However, an assay for CR 1 ‐mediated IC binding showed a clearly reduced E‐CR1 function.