The Effect of Intravenous γ-Globulin on the Induction of Experimental Antiphospholipid Syndrome

Bakimer, R.; Guilburd, B.; Zurgil, N.; Shoenfeld, Yehuda

doi:10.1006/clin.1993.1155

Cited by 86 publications

(54 citation statements)

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“…The human anti-␤2GPI mAbs designated ILA-1 and ILA-3 (IgMs) were prepared by the human-human hybridoma technique from a patient with APS (17). The H-3 mAb was prepared as previously described (19). All three anti-␤2GPI mAbs were found to activate ECs in vitro and to induce experimental APS by passive transfer (17,19).…”

Section: Methodsmentioning

confidence: 99%

“…The H-3 mAb was prepared as previously described (19). All three anti-␤2GPI mAbs were found to activate ECs in vitro and to induce experimental APS by passive transfer (17,19).…”

Section: Methodsmentioning

confidence: 99%

“…The anti-␤2GPI mAbs ILA-1, ILA-3, and H-3, at 50% binding (corresponding to 5, 3.5, and 5 g͞ml respectively), were incubated with varying concentrations of the peptides A, B, and C, respectively. The reaction mixture was then transferred to the ␤2GPI-coated plates and assayed as described (17,19). The percentage of inhibition was calculated as follows: % inhibition ϭ [OD anti-␤2GPI-OD anti-␤2GPI with inhibitor]͞OD anti-␤2GPI ϫ100.…”

Section: Methodsmentioning

confidence: 99%

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Prevention of experimental antiphospholipid syndrome and endothelial cell activation by synthetic peptides

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Shoenfeld

Cabilly

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

165

136

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Antiphospholipid syndrome (APS) is characterized by recurrent fetal loss, repeated thromboembolic phenomena, and thrombocytopenia. The syndrome is believed to be caused by antiphospholipid beta-2-glycoprotein-I (␤2GPI)-dependent Abs or anti-␤2GPI Abs by themselves. Using a hexapeptide phage display library, we identified three hexapeptides that react specifically with the anti-␤2GPI mAbs ILA-1, ILA-3, and H-3, which cause endothelial cell activation and induce experimental APS. To enhance the binding of the peptides to the corresponding mAbs, the peptides were lengthened to correspond with the site of the ␤2GPI epitope being recognized by these mAbs. As a result, the following three peptides were prepared: A, NTLKTPRVGGC, which binds to ILA-1 mAb; B, KDKATFGCHDGC, which binds to ILA-3 mAb; and C, CATLRVYKGG, which binds to H-3 mAb. Peptides A, B, and C specifically inhibit both in vitro and in vivo the biological functions of the corresponding anti-␤2GPI mAbs. Exposure of endothelial cells to anti-␤2GPI mAbs and their corresponding peptides led to the inhibition of endothelial cell activation, as shown by decreased expression of adhesion molecules (E-selectin, ICAM-1, VCAM-1) and monocyte adhesion. In vivo infusion of each of the anti-␤2GPI mAbs into BALB͞c mice, followed by administration of the corresponding specific peptides, prevented the peptide-treated mice from developing experimental APS. The use of synthetic peptides that focus on neutralization of pathogenic anti-␤2GPI Abs represents a possible new therapeutic approach to APS.

show abstract

Section: Methodsmentioning

confidence: 99%

“…The H-3 mAb was prepared as previously described (19). All three anti-␤2GPI mAbs were found to activate ECs in vitro and to induce experimental APS by passive transfer (17,19).…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Prevention of experimental antiphospholipid syndrome and endothelial cell activation by synthetic peptides

Blank

Shoenfeld

Cabilly

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

165

136

View full text Add to dashboard Cite

show abstract

“…There is little information regarding the teratogenicity of IVIG in animals. One report showed that IVIG was well tolerated in pregnant mice with induced antiphospholipid antibody syndrome (Bakimer 1993). In humans, IVIG appears to cross the placenta after 32 weeks of gestation, even after modification that alters the Fc binding sites ( Hockel 1986).…”

Section: Intravenous Immune Globulins (Ivig)mentioning

confidence: 99%

Sexual and Reproductive Function in Chronic Kidney Disease and Effect of Kidney Transplantation

Lessan‐Pezeshki¹,

Ghazizadeh²

2011

After the Kidney Transplant - The Patients and Their Allograft

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“…How can we relate the experimental induction of autoimmune disease in mice to human autoimmune disease according to the idiotypic dysregulation theory? It is possible that pathogenic idiotypes of autoantibodies may be present not only on autoantibodies but also on anti-bacterial or anti-viral antibodies [26], Indeed, previously we demonstrated the presence of the 16/6 anti-DNA idiotype in sera of patients with active pulmonary tuberculosis [27] and patients with klebsiella infections. The presence of pathogenic idiotypes on antibacterial antibodies in association with a bacterial adjuvant etTecl may precipitate a chain of events leading to the production of Ab3 and eventually to the emergence of classical autoimmune disease manifestations and the disease related autoantibodies in a subject with the "proper" genetic background or with other risk factors.…”

Section: Induction Ofthe Following Immunization With Idiotype Emulsifmentioning

confidence: 89%

Idiotypic network, pathogenic autoantibodies and autoimmunity

Shoenfeld

1995

Clinical and Experimental Immunology

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The Effect of Intravenous γ-Globulin on the Induction of Experimental Antiphospholipid Syndrome

Cited by 86 publications

References 0 publications

Prevention of experimental antiphospholipid syndrome and endothelial cell activation by synthetic peptides

Prevention of experimental antiphospholipid syndrome and endothelial cell activation by synthetic peptides

Sexual and Reproductive Function in Chronic Kidney Disease and Effect of Kidney Transplantation

Idiotypic network, pathogenic autoantibodies and autoimmunity

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