Application of Monoclonal Antibodies to Issues of Plasma Lipoprotein Structure and Function

Curtiss, Linda K.

doi:10.1007/978-1-4684-4964-8_17

Cited by 3 publications

(1 citation statement)

References 44 publications

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“…Apo E in the culture medium was assayed immunochemically in a sensitive competitive solid-phase radioimmunoassay. Microtiter plates were precoated with 0.1 ml of protein A at 500 ng/ml in borate-buffered saline and then coated with the apo E-specific monoclonal antibody, lE (17). The IE antibody is an IgG2a k antibody, which was generated from the fusion of P3.Ag8.653.…”

Section: Methodsmentioning

confidence: 99%

New mechanism for foam cell generation in atherosclerotic lesions.

et al. 1987

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Section: Methodsmentioning

confidence: 99%

New mechanism for foam cell generation in atherosclerotic lesions.

et al. 1987

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What causes the antiphospholipid syndrome?

Merrill

2001

Curr Rheumatol Rep

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The antiphospholipid syndrome (APS) is characterized by unpredictable, sporadic, thrombotic events. The cause of the thrombosis is probably multifactorial and may involve disparate effects of the autoantibodies associated with the syndrome, which are known to interfere with various protein regulators of hemostasis. An integrated theory of pathogenesis that accounts for the diversity of autoantibodies and their effects suggests that cellular inflammation or apoptosis within the vasculature may lead to oxidation or turnover in phospholipid membranes. Thus, normally cryptic, functionally important epitopes of phospholipid-binding proteins are subjected to increased exposure to immune surveillance.

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Fequency of antibodies to the cholesterol transport protein apolipoprotein A1 in patients with SLE

Dinu¹,

Merrill²,

Shen

et al. 1998

Lupus

106

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In examining reasons for premature atherosclerosis in systemic lupus erythematosus (SLE), we previously reported low levels of the cholesterol transport protein apolipoprotein A1 (apoA1) in these patients, and specific antibodies to purified apoA1 were identified in the sera of 5 out of 30 lupus patients. The current study was initiated to determine whether these antibodies are common in lupus patients. 520 serum samples from 175 patients with SLE or primary antiphospholipid syndrome (PAPS) were tested for antibodies to purified apoA1. Positive sera were retested for binding to apolipoprotein incorporated into reconstructed nascent or mature high-density lipoprotein (HDL). Autoantibodies to apoA1 were found in 32.5% of patients with SLE and 22.9% of patients with PAPS, associated with the presence of aPL (anti-beta2 glycoprotein-1, anti-beta2 GP1) antibodies. When reconstructed, nascent and mature HDL molecules were compared as antigen-containing environments, positive sera reacted best to apoA1 embedded in mature HDL molecules. This report confirms the high prevalence of antibodies to apoA1 in patients with systemic lupus and suggests a high affinity of these antibodies for mature HDL.

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Application of Monoclonal Antibodies to Issues of Plasma Lipoprotein Structure and Function

Cited by 3 publications

References 44 publications

New mechanism for foam cell generation in atherosclerotic lesions.

New mechanism for foam cell generation in atherosclerotic lesions.

What causes the antiphospholipid syndrome?

Fequency of antibodies to the cholesterol transport protein apolipoprotein A1 in patients with SLE

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