LAD-III, a novel group of leukocyte integrin activation deficiencies

被引:71
作者
Alon, R [1 ]
Etzioni, A
机构
[1] Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel
[2] Technion Israel Inst Technol, Rambam Med Ctr, Meyer Children Hosp, Dept Pediat, IL-31096 Haifa, Israel
[3] Technion Israel Inst Technol, B Rappaport Sch Med, IL-31096 Haifa, Israel
基金
以色列科学基金会;
关键词
D O I
10.1016/j.it.2003.08.001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
To extravasate the bloodstream at specific targets, circulating immune cells must activate their integrins to undergo rapid in situ modulation of affinity or avidity for their endothelial ligands. This activation involves specialized sub-second G-protein signal transduction triggered by endothelium-displayed chemo-attractants-primarily chemokines-and their cognate leukocyte-expressed G-protein-coupled receptors (GPCRs). Recently, we reported a rare autosomal-recessive leukocyte adhesion deficiency (LAD) syndrome associated with a defective ability of integrins to undergo GPCR-mediated stimulation at endothelial contacts. This LAD shows significant similarities to a group of integrin-activation syndromes reported in leukocytes and platelets. Here, the mechanisms by which GPCRs might regulate leukocyte and platelet integrins are outlined with respect to this new family of LAD cases. We propose to term this the LAD-III family.
引用
收藏
页码:561 / 566
页数:6
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