Induction of thrombosis in a mouse model by IgG, IgM and IgA immunoglobulins from patients with the antiphospholipid syndrome
Abstract
Antiphospholipid syndrome is a disorder of recurrent thrombosis and pregnancy losses associated with production of anticardiolipin antibodies and lupus anticoagulant positivity. Recently, we have adapted a mouse model of induced venous thrombosis to study the role of autoantibodies in thrombus formation. To determine whether immunoglobulins from patients with the antiphospholipid syndrome play a role in thrombosis, we injected groups of CDI mice either with immunoglobulins purified from seven patients with the antiphospholipid syndrome (nine preparations studied: four IgG, three IgM and two IgA) or with immunoglobulins of the same isotype from healthy controls. Seventy-two h after injection, a non-occlusive thrombus was induced in the femoral veins of experimental mice by a pinch injury; the thrombus areas as well as times of formation and disappearance of the thrombi were measured. Eight of the nine antiphospholipid syndrome immunoglobulin preparations caused a significant increase in mean thrombus area and a significant delay in mean thrombus disappearance time as compared with normal controls. To determine whether anticardiolipin antibodies might be involved, separate groups of mice were injected with affinity-purified IgG (n = 2) or IgM (n = 2) anticardiolipin antibodies or with normal immunoglobulins of the same isotype, and the effects on thrombus formation compared. Mean thrombus area and mean disappearance times were again significantly increased in all four groups injected with affinity-purified antibodies. This is the first study to show that anticardiolipin antibodies of IgG, IgM and IgA isotypes may play a role in thrombosis in vivo.
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Elevated titres of IgA isotypes have been shown to be associated with thrombosis.
“Moreover, elevated titres of IgA isotypes have been shown to be associated with thrombosis [10, 14–16].”
From Antiphospholipid patterns predict risk of thrombosis in systemic lupus erythematosus (2021) · cites this paper as [14]
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- Authors
- Pierangeli, S. S., Liu, X. W., Barker, J. H., Anderson, G., & Harris, E. N.
- Affiliations
- The Antiphospholipid Standardization Laboratory, Louisville, KY, USA
- The Department of Medicine, Division of Rheumatology, Louisville, KV, USA
- The Department of Surgery, Louisville, KY, USA
- University of Louisville (US)
- Venue
- Thrombosis and Haemostasis
- Publisher
- Georg Thieme Verlag KG
- Published
- 1995
- Volume
- 74
- Issue
- 05
- Pages
- 1361-1367
- ISSN
- 0340-6245 (ISSN-L)
- 2567-689X
- OpenAlex
- W167774609
- Cited by
- 223
- References
- 45
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 7 · 2023: 2 · 2022: 5 · 2021: 2 · 2020: 8 · 2019: 7 · 2018: 4 · 2017: 7 · 2016: 10 · 2015: 4 · 2014: 4 · 2013: 9 · 2012: 13
- FWCI
- 5.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Thrombosis and Haemostasis (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
- Health Sciences › Medicine › Hematology › Platelet Disorders and Treatments
- Keywords
- antiphospholipid syndrome, anticardiolipin antibodies, thrombosis, IgG, immunoglobulin M, immunoglobulin A, autoantibodies, venous thrombosis, mouse model, ICR mice, lupus anticoagulant, thrombus formation
- MeSH terms
- Animals, Femoral Vein, Humans, Immunoglobulin A, Immunoglobulin G, Immunoglobulin M, Immunization, Passive, Male, Thrombosis, Antiphospholipid Syndrome, Mice
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