Natural antibodies against phosphorylcholine as potential protective factors in SLE.
OBJECTIVE
We have recently reported that natural antibodies against phosphorylcholine (anti-PC) have atheroprotective properties. Here we compare anti-PC with other autoantibodies in SLE patients with and without cardiovascular disease (CVD).


METHODS
Twenty-six women (52 +/- 8.2 yrs) with SLE and a history of CVD (SLE cases) were compared with 26 age-matched women with SLE without CVD (SLE controls) and 26 age-matched population-based control women (controls). PC was conjugated with BSA (PC-BSA) or keyhole-limpet haemocyanin (PC-KLH). Anti-PC and antibodies against phosphatidylserine (anti-PS) and BSA (anti-BSA) were studied by ELISA. Anti-PC-IgG were extracted from intravenous immunoglobulin (IVIG). Activation of endothelial cells by platelet-activating factor (PAF) was studied with FACScan.


RESULTS
IgG anti-PC-BSA and anti-PC-KLH were decreased among SLE-cases and SLE-controls as compared with controls (P < 0.005 and P < 0.05), respectively. SLE cases were more prevalent in the lowest 25th percentile of anti-PC-IgM (and IgG) as compared with controls (P < 0.05) but anti-PC-IgM levels did not differ significantly between groups. Among SLE controls, anti-PC-BSA were associated negatively with organ damage (SLICC) and disease activity (SLEDAI) (P < 0.05). Among SLE cases, anti-PC-BSA and anti-PC-KLH were associated negatively with SLICC (P = 0.021; P = 0.010) and anti-PC-BSA was negatively associated with SLEDAI (P < 0.039). Anti-PS-IgG and anti-BSA-IgG were raised among SLE cases as compared with other groups (P < 0.05) and did not cross-react with anti-PC. Anti-PC-IgG could be extracted from IVIG and inhibited PAF-induced expression of adhesion molecules.


CONCLUSIONS
Low levels of anti-PC could be of importance in SLE. Anti-BSA and anti-PS and low levels of anti-PC could contribute to development of CVD in SLE.
Rheumatology Unit, Karolinska University Hospital, Huddinge, Karolinska Institutet [corrected] Stockholm, Sweden. jun.su@ki.se
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J
Su
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Hua
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Concha
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Svenungsson
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Cederholm
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Frostegård
D000328:Adult; D001323:Autoantibodies / Q000097:blood*; D001667:Binding, Competitive; D002318:Cardiovascular Diseases / Q000209:etiology / Q000276:immunology; D003429:Cross Reactions; D004730:Endothelium, Vascular / Q000276:immunology; D005260:Female; D006433:Hemocyanins / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000276:immunology*; D008875:Middle Aged; D010767:Phosphorylcholine / Q000031:analogs & derivatives / Q000276:immunology*; D010972:Platelet Activating Factor / Q000276:immunology; D012710:Serum Albumin, Bovine / Q000276:immunology; D012720:Severity of Illness Index; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
D001323:Autoantibodies; D007074:Immunoglobulin G; D010972:Platelet Activating Factor; D019010:Vascular Cell Adhesion Molecule-1; C076110:phosphorylcholine-bovine serum albumin; D010767:Phosphorylcholine; D018799:Intercellular Adhesion Molecule-1; D012710:Serum Albumin, Bovine; D006433:Hemocyanins; C032808:keyhole-limpet hemocyanin