Immune mechanisms in heparin‐induced thrombocytopenia: no evidence for immunoglobulin M anti‐idiotype antibodies
Immune mechanisms in heparin‐induced thrombocytopenia: no evidence for immunoglobulin M anti‐idiotype antibodies
复制标题
肝素诱导的血小板减少症的免疫机制：没有免疫球蛋白 M 抗独特型抗体的证据
作者：
K. Selleng;T. Warkentin;J. Sheppard;A. Greinacher
背景：肝素诱导的血小板减少症(HIT)是由抗血小板第4因子(PF4)/肝素复合体的血小板(PLT)激活免疫球蛋白(Ig)G抗体引起的，与免疫血液学中的其他免疫反应不同：即使没有接触过肝素，Ig抗体也最早在5天内形成；抗体具有明显的暂时性(100天)；尽管使用相同类型和剂量的肝素，但术后患者HIT比内科患者更常见；越来越多的证据表明抗PF4/肝素抗体具有自身抗体样反应。我们推测，这些不寻常的特征可能是由于独特型-抗独特型网络的干扰(例如，手术)导致的调节性抗独特型IgM抗体的丢失。
BACKGROUND: Heparin‐induced thrombocytopenia (HIT), which is caused by platelet (PLT)‐activating immunoglobulin (Ig)G antibodies against platelet factor 4 (PF4)/heparin complexes, differs from other immune responses seen in immunohematology: IgG antibodies are formed as early as 5 days even without previous heparin exposure; antibodies are remarkably transient (<100 days); HIT is more frequent in postsurgery patients compared with medical patients despite administering the same type and dose of heparin; and increasing evidence implicates autoantibody‐like reactivity of anti‐PF4/heparin antibodies. We hypothesized that these unusual features could be caused by loss of regulatory anti‐idiotype IgM antibodies due to disturbance (e.g., by surgery) of an idiotype–anti‐idiotype network.
影响因子：
158.5
作者：
Amanna, Ian J.;Carlson, Nichole E.;Slifka, Mark K.
通讯作者：
Slifka, Mark K.
影响因子：
20.3
作者：
Rauova, L;Zhai, L;Poncz, M
通讯作者：
Poncz, M
肝素诱导的血小板减少症的小鼠模型。
DOI：
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发表时间：
1999
期刊：
Seminars in hematology.
影响因子：
--
作者：
Blank,M;Eldor,A;Tavor,S;Ziporen,L;Cines,DB;Arepally,G;Afek,A;Shoenfeld,Y
通讯作者：
Shoenfeld,Y