Antiphospholipid syndrome: insights from animal models

被引:13
作者
Sherer, Y
Shoenfeld, Y [1 ]
机构
[1] Dept Med B, IL-52621 Tel Hashomer, Israel
[2] Chaim Sheba Med Ctr, Autoimmune Dis Res Unit, IL-52621 Tel Hashomer, Israel
[3] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel
关键词
D O I
10.1097/00062752-200009000-00011
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Animal models of the relatively new anti phospholipid syndrome (APS) enabled researchers to understand disease pathogenesis and to test novel experimental therapeutic modalities. Animal models of APE include spontaneous genetic models and experimental induced models. The latter test more reliably the pathogenicity of antiphospholipid antibodies because the syndrome is induced in normal mice rather than being secondary to a preexisting autoimmune disease. Reports about animal models of APS in the recent year provide new insights into the pathogenesis of antiphospholipid antibodies and beta2-glycoprotein-I in reproductive failure, neurologic manifestations, thrombosis and atherosclerosis. In addition, novel therapies that were successful in experimental APS included anti-idiotypes, oral tolerance, and specific peptides that bind to beta2-glycoprotein-I. Animal models provide the first step in development of novel therapies for patients with APS. (C) 2000 Lippincott Williams & Wilkins, Inc.
引用
收藏
页码:321 / 324
页数:4
相关论文
共 15 条
[1]   INDUCTION OF PRIMARY ANTIPHOSPHOLIPID SYNDROME IN MICE BY IMMUNIZATION WITH A HUMAN MONOCLONAL ANTICARDIOLIPIN ANTIBODY (H-3) [J].
BAKIMER, R ;
FISHMAN, P ;
BLANK, M ;
SREDNI, B ;
DJALDETTI, M ;
SHOENFELD, Y .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 89 (05) :1558-1563
[2]   Prevention of experimental antiphospholipid syndrome and endothelial cell activation by synthetic peptides [J].
Blank, M ;
Shoenfeld, Y ;
Cabilly, S ;
Heldman, Y ;
Fridkin, M ;
Katchalski-Katzir, E .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (09) :5164-5168
[3]  
Blank M, 1998, J IMMUNOL, V161, P5303
[4]   INDUCTION OF ANTIPHOSPHOLIPID SYNDROME IN NAIVE MICE WITH MOUSE LUPUS MONOCLONAL AND HUMAN POLYCLONAL ANTICARDIOLIPIN ANTIBODIES [J].
BLANK, M ;
COHEN, J ;
TODER, V ;
SHOENFELD, Y .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (08) :3069-3073
[5]   Antiphospholipid antibodies permeabilize and depolarize brain synaptoneurosomes [J].
Chapman, J ;
Cohen-Armon, M ;
Shoenfeld, Y ;
Korczyn, AD .
LUPUS, 1999, 8 (02) :127-133
[6]   Immunolocalization of β2 glycoprotein I (apolipoprotein H) to human atherosclerotic plaques -: Potential implications for lesion progression [J].
George, J ;
Harats, D ;
Gilburd, B ;
Afek, A ;
Levy, Y ;
Schneiderman, J ;
Barshack, I ;
Kopolovic, J ;
Shoenfeld, Y .
CIRCULATION, 1999, 99 (17) :2227-2230
[7]   Induction of early atherosclerosis in LDL-receptor-deficient mice immunized with β2-glycoprotein I [J].
George, J ;
Afek, A ;
Gilburd, B ;
Blank, M ;
Levy, Y ;
Aron-Maor, A ;
Levkovitz, H ;
Shaish, A ;
Goldberg, I ;
Kopolovic, J ;
Harats, D ;
Shoenfeld, Y .
CIRCULATION, 1998, 98 (11) :1108-1115
[8]   The involvement of β2-glycoprotein I (β2-GPI) in human and murine atherosclerosis [J].
George, J ;
Shoenfeld, Y ;
Harats, D .
JOURNAL OF AUTOIMMUNITY, 1999, 13 (01) :57-60
[9]  
Gharavi AE, 1999, J IMMUNOL, V163, P2922
[10]   Induction of antiphospholipid antibodies by immunization with synthetic viral and bacterial peptides [J].
Gharavi, EE ;
Chaimovich, H ;
Cucurull, E ;
Celli, CM ;
Tang, H ;
Wilson, WA ;
Gharavi, AE .
LUPUS, 1999, 8 (06) :449-455