Anticardiolipin antibodies in NZW x BXSB F1 mice

A model of antiphospholipid syndrome

Yoshiko Hashimoto, Masayo Kawamura, Kenji Ichikawa, Takahiro Suzuki, Takayuki Sumida, Sho Yoshida, Eiji Matsuura, Susumu Ikehara, Takao Koike

Research output: Contribution to journalArticle

153 Citations (Scopus)

Abstract

NZW x BXSB F1 (W/B F1) male mice develop systemic lupus-like disease, and several autoantibodies, circulating immune complexes, and lupus nephritis become apparent. The abnormally high incidence of degenerative coronary vascular disease with myocardial infarction and thrombocytopenia due to the presence of both platelet-associated antibodies and circulating antiplatelet antibodies in this animal has been reported. We found that W/B F1 male mice produced autoantibodies against cardiolipin (aCL) and that the titer of aCL increases with age. aCL from W/B F1 male mice were mainly IgG and binding activity to cardiolipin was aCL-cofactor (β2-glycoprotein I (β2-GPI)) dependent. We developed monoclonal aCL from these animals and examined specificity of the autoantibodies. All the mAb used reacted with the negatively charged phospholipids, cardiolipin, phosphatidylserine, and phosphatidylinositol, and some reacted with platelets and DNA. The addition of human or mouse β2-GPI enhanced the titer for monoclonal aCL from the W/B F1 mice. From the results of competitive inhibition enzyme immunoassay with monoclonal aCL and purified β2-GPI, aCL from the W/B F1 mice recognized the complex of CL and β2-GPI. The W/B F1 male mouse may be an appropriate model for use in studies on the pathologic significance of aCL in patients with antiphospholipid syndrome.

Original languageEnglish
Pages (from-to)1063-1068
Number of pages6
JournalJournal of Immunology
Volume149
Issue number3
Publication statusPublished - Aug 1 1992
Externally publishedYes

Fingerprint

Anticardiolipin Antibodies
Cardiolipins
Antiphospholipid Syndrome
Glycoproteins
Autoantibodies
Blood Platelets
Lupus Nephritis
Antibodies
Phosphatidylserines
Phosphatidylinositols
Antigen-Antibody Complex
Immunoenzyme Techniques
Vascular Diseases
Thrombocytopenia
Coronary Disease
Phospholipids
Immunoglobulin G
Myocardial Infarction

ASJC Scopus subject areas

  • Immunology

Cite this

Hashimoto, Y., Kawamura, M., Ichikawa, K., Suzuki, T., Sumida, T., Yoshida, S., ... Koike, T. (1992). Anticardiolipin antibodies in NZW x BXSB F1 mice: A model of antiphospholipid syndrome. Journal of Immunology, 149(3), 1063-1068.

Anticardiolipin antibodies in NZW x BXSB F1 mice : A model of antiphospholipid syndrome. / Hashimoto, Yoshiko; Kawamura, Masayo; Ichikawa, Kenji; Suzuki, Takahiro; Sumida, Takayuki; Yoshida, Sho; Matsuura, Eiji; Ikehara, Susumu; Koike, Takao.

In: Journal of Immunology, Vol. 149, No. 3, 01.08.1992, p. 1063-1068.

Research output: Contribution to journalArticle

Hashimoto, Y, Kawamura, M, Ichikawa, K, Suzuki, T, Sumida, T, Yoshida, S, Matsuura, E, Ikehara, S & Koike, T 1992, 'Anticardiolipin antibodies in NZW x BXSB F1 mice: A model of antiphospholipid syndrome', Journal of Immunology, vol. 149, no. 3, pp. 1063-1068.
Hashimoto Y, Kawamura M, Ichikawa K, Suzuki T, Sumida T, Yoshida S et al. Anticardiolipin antibodies in NZW x BXSB F1 mice: A model of antiphospholipid syndrome. Journal of Immunology. 1992 Aug 1;149(3):1063-1068.
Hashimoto, Yoshiko ; Kawamura, Masayo ; Ichikawa, Kenji ; Suzuki, Takahiro ; Sumida, Takayuki ; Yoshida, Sho ; Matsuura, Eiji ; Ikehara, Susumu ; Koike, Takao. / Anticardiolipin antibodies in NZW x BXSB F1 mice : A model of antiphospholipid syndrome. In: Journal of Immunology. 1992 ; Vol. 149, No. 3. pp. 1063-1068.
@article{4e7a841047cf4b2e9f1ebf054dfbf876,
title = "Anticardiolipin antibodies in NZW x BXSB F1 mice: A model of antiphospholipid syndrome",
abstract = "NZW x BXSB F1 (W/B F1) male mice develop systemic lupus-like disease, and several autoantibodies, circulating immune complexes, and lupus nephritis become apparent. The abnormally high incidence of degenerative coronary vascular disease with myocardial infarction and thrombocytopenia due to the presence of both platelet-associated antibodies and circulating antiplatelet antibodies in this animal has been reported. We found that W/B F1 male mice produced autoantibodies against cardiolipin (aCL) and that the titer of aCL increases with age. aCL from W/B F1 male mice were mainly IgG and binding activity to cardiolipin was aCL-cofactor (β2-glycoprotein I (β2-GPI)) dependent. We developed monoclonal aCL from these animals and examined specificity of the autoantibodies. All the mAb used reacted with the negatively charged phospholipids, cardiolipin, phosphatidylserine, and phosphatidylinositol, and some reacted with platelets and DNA. The addition of human or mouse β2-GPI enhanced the titer for monoclonal aCL from the W/B F1 mice. From the results of competitive inhibition enzyme immunoassay with monoclonal aCL and purified β2-GPI, aCL from the W/B F1 mice recognized the complex of CL and β2-GPI. The W/B F1 male mouse may be an appropriate model for use in studies on the pathologic significance of aCL in patients with antiphospholipid syndrome.",
author = "Yoshiko Hashimoto and Masayo Kawamura and Kenji Ichikawa and Takahiro Suzuki and Takayuki Sumida and Sho Yoshida and Eiji Matsuura and Susumu Ikehara and Takao Koike",
year = "1992",
month = "8",
day = "1",
language = "English",
volume = "149",
pages = "1063--1068",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "3",

}

TY - JOUR

T1 - Anticardiolipin antibodies in NZW x BXSB F1 mice

T2 - A model of antiphospholipid syndrome

AU - Hashimoto, Yoshiko

AU - Kawamura, Masayo

AU - Ichikawa, Kenji

AU - Suzuki, Takahiro

AU - Sumida, Takayuki

AU - Yoshida, Sho

AU - Matsuura, Eiji

AU - Ikehara, Susumu

AU - Koike, Takao

PY - 1992/8/1

Y1 - 1992/8/1

N2 - NZW x BXSB F1 (W/B F1) male mice develop systemic lupus-like disease, and several autoantibodies, circulating immune complexes, and lupus nephritis become apparent. The abnormally high incidence of degenerative coronary vascular disease with myocardial infarction and thrombocytopenia due to the presence of both platelet-associated antibodies and circulating antiplatelet antibodies in this animal has been reported. We found that W/B F1 male mice produced autoantibodies against cardiolipin (aCL) and that the titer of aCL increases with age. aCL from W/B F1 male mice were mainly IgG and binding activity to cardiolipin was aCL-cofactor (β2-glycoprotein I (β2-GPI)) dependent. We developed monoclonal aCL from these animals and examined specificity of the autoantibodies. All the mAb used reacted with the negatively charged phospholipids, cardiolipin, phosphatidylserine, and phosphatidylinositol, and some reacted with platelets and DNA. The addition of human or mouse β2-GPI enhanced the titer for monoclonal aCL from the W/B F1 mice. From the results of competitive inhibition enzyme immunoassay with monoclonal aCL and purified β2-GPI, aCL from the W/B F1 mice recognized the complex of CL and β2-GPI. The W/B F1 male mouse may be an appropriate model for use in studies on the pathologic significance of aCL in patients with antiphospholipid syndrome.

AB - NZW x BXSB F1 (W/B F1) male mice develop systemic lupus-like disease, and several autoantibodies, circulating immune complexes, and lupus nephritis become apparent. The abnormally high incidence of degenerative coronary vascular disease with myocardial infarction and thrombocytopenia due to the presence of both platelet-associated antibodies and circulating antiplatelet antibodies in this animal has been reported. We found that W/B F1 male mice produced autoantibodies against cardiolipin (aCL) and that the titer of aCL increases with age. aCL from W/B F1 male mice were mainly IgG and binding activity to cardiolipin was aCL-cofactor (β2-glycoprotein I (β2-GPI)) dependent. We developed monoclonal aCL from these animals and examined specificity of the autoantibodies. All the mAb used reacted with the negatively charged phospholipids, cardiolipin, phosphatidylserine, and phosphatidylinositol, and some reacted with platelets and DNA. The addition of human or mouse β2-GPI enhanced the titer for monoclonal aCL from the W/B F1 mice. From the results of competitive inhibition enzyme immunoassay with monoclonal aCL and purified β2-GPI, aCL from the W/B F1 mice recognized the complex of CL and β2-GPI. The W/B F1 male mouse may be an appropriate model for use in studies on the pathologic significance of aCL in patients with antiphospholipid syndrome.

UR - http://www.scopus.com/inward/record.url?scp=0026777054&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026777054&partnerID=8YFLogxK

M3 - Article

VL - 149

SP - 1063

EP - 1068

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 3

ER -