A need for standardization of the anti-endothelial-cell antibody test

doi:10.1016/0167-5699(95)80001-8

Immunology Today

Volume 16, Issue 8, August 1995, Pages 363-364

https://doi.org/10.1016/0167-5699(95)80001-8 Get rights and content

Abstract

Anti-endothelial-cell antibodies (AECAs) have been described in a number of conditions. However, the exact prevalence of AECAs is not yet known because of the considerable variation in results obtained by different investigators. A recent meeting¹

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Endothelial Cell Autoreactivity and Infection
2015, Infection and Autoimmunity
Antiendothelial cell antibodies (AECAs) are detected in a number of infectious diseases, but their pathogenic role remains unclear. As a result of damaging the target cells, Mycobacterium leprae and dengue virus trigger the production of such endothelial cell-specific autoantibodies. Other infectious agents, including malaria and the Epstein–Barr virus, generate polyclonal B cell activation and thereby nonspecific AECAs. Endothelial cell-specific AECAs recognize membrane antigens, whereas nonspecific AECAs are directed against cytosol components. The former antibodies, but not the latter, activate the cells and induce apoptosis. Studies, using two-dimensional electrophoresis and expression banks have contributed to the identification of the cell surface epitope(s), including endogenous heat stock proteins that cross-react with bacterial components.
Endothelium, a target for immune-mediated assault in connective tissue disease
2006, Autoimmunity Reviews
Evidence is lacking that antibodies (Ab) to endothelial cells (AECA) are pathogenic. They are frequently associated with antiphospholipid Ab (aPL), binding to complexes of phosphatidylserine (PS) with β2GPI. Recent studies have, however, kindled a new debate on their pathogenicity of AECA. A group is responsible for PS reaching the surface of a cell, a feature of commitment to apoptosis. Defective clearance by macrophages of AECA-induced apoptotic cells might display β2GPI on their surface, and challenge T cell tolerance, until aPL production. Some AECA are thus induced by cell membrane structures, while others recognize “planted” antigens and possibly ligand–receptor complexes. A second group promotes procoagulant factor, and a third has the capacity to trigger apoptosis. Clearly, the most direct demonstration of the pathogenicity of AECA is the autoAb-induced murine model of vasculiltis.
New target antigens for antiendothelial cell antibodies
2005, Immunobiology
Numerous connective tissue diseases, such as systemic lupus erythematosus (SLE), and infectious states, such as leprosy, are characterized by early vascular endothelial cell (EC) damage. There is substantial interest in the role of anti-EC antibodies (AECA) in such an injury. Due to the diversity of AECA-associated conditions, these autoantibodies are likely to be heterogeneous, and, therefore, identification of their antigens (Ag) to be difficult. They may be classified into three groups: membrane components, ligand–receptor complexes and Ag derived from the blood and attached to the cell surface. New technologies have been developed to sort it out, such as expression libraries and two-dimensional electrophoresis. A handful of Ag have hitherto been recognized viz. heat-shock protein 60 in SLE and leprosy, or plasminogen activator inhibitor-1 in SLE and Wegener granulomatosis. In reality, most of the target Ag for AECA remain to be identified.
Humoral autoimmunity against endothelium: Theory or reality?
2005, Trends in Immunology
Despite the discovery of anti-endothelial cell antibodies (AECA) in a heterogeneous group of disorders characterized by endothelial damage, their pathogenic role is still debated. Experimental in vitro models indicate that they can either damage endothelial cells or trigger cell signaling by reacting with as yet undefined surface molecules. However, clinical studies suggest that, in addition to AECA, other pathogenic mechanisms are involved in the vasculitic process. Recently, antibodies specific for β2 glycoprotein I, the phospholipid-binding protein targeted by anti-phospholipid antibodies, have been shown to display anti-endothelial activity. These autoantibodies recognize β2 glycoprotein I adhered to the endothelium and induce a cell perturbation that might underlie the thrombophilic state of the anti-phospholipid syndrome.
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2004, Infection and Autoimmunity, 2nd edition
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2003, International Journal of Cardiology
Coronary heart disease clusters within families, but there may be several reasons for this phenomenon to occur. A possible way to elucidate this is to study biological relatives of affected individuals. The aim of our study was thus to compare a number of clinical, metabolic, clotting and immunologic factors between offspring with paternal history of premature myocardial infarction and controls and to propose a model which could safely allow to identify the high risk subgroup among them. Sixty-nine offspring of both sexes mean age 18.1 years old (cases) and thirty-two frequency matched relative to age and gender controls were studied. Cases compared to controls had significantly increased diastolic blood pressure levels (74.0±9.9 vs. 67.4±8.3 mmHg, P=0.002), leptin plasma levels (11.8±10.8 vs. 6.8±3 ng/ml, P=0.046) and fibrinogen, plasminogen, fibrin degradation products and plasminogen activator inhibitor-1 plasma levels (306.6±52.5 vs. 280.6±28.9 mg%, P=0.03, 97.4±23.5 vs. 83.6±15 mg%, P=0.0007, 292.0±148.5 vs. 219.2±69.4 ng/ml, P=0.036, 14.7±5.3 vs. 8.7±3.1 I.U./ml, P=0.0001, respectively), while cases had significantly decreased HDL-cholesterol serum levels (45.9±12.5 vs. 50.5±8.8 mg%, P=0.03) and protein S plasma levels (89.9±17.5 vs. 101.3±13.7%, P=0.001). Our findings suggest that offspring of affected individuals may be considered as a high risk group for cardiovascular disease.

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¹: The Workshop ‘Anti-Endothelial-Cell Antibodies’ was part of the 4th International Conference on SLE, and was held in Jerusalem, Israel, on 26–31 March 1995.

²: Pierre Youinou is at the Laboratory of Immunology, Brest University Medical School, 29609 Brest France

³: Pier-Luigi Meroni is at the Istituto di Medicina Interna, Ospedale Policlinico, 20122 Milano, Italy

⁴: Munther Khamashta is at the Rayne Institute, St Thomas' Hospital, London, UK SE1 7E11

⁵: Yehuda Shoenfeld is at the Sheba Medical Centre, Tel-Hashomer 52621, Israel.

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A need for standardization of the anti-endothelial-cell antibody test

Abstract

Clin. Exp. Immunol.

Arthritis Rheum.

J. Clin. Invest.

Lupus

Proc. Natl Acad. Sci. USA