The heat-stable antigen can alter very late antigen 4-mediated adhesion.
The heat-stable antigen can alter very late antigen 4-mediated adhesion.
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DOI：
10.1084/jem.179.4.1391
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发表时间：
1994-04-01
期刊：
影响因子：
--
通讯作者：
Nielsen PJ
中科院分区：
文献类型：
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作者：
Hahne M;Wenger RH;Vestweber D;Nielsen PJ
整联蛋白极晚期抗原（VLA-4）α 4 β 1及其反受体血管细胞粘附分子1（VCAM-1）参与B细胞成熟和前B细胞与骨髓基质细胞的附着。我们已经分析了是否热稳定抗原（HSA），未成熟白细胞的标志物，参与这种细胞粘附现象。HSA是一种糖脂锚定的高度糖基化的表面蛋白，在造血系统和神经系统的成熟过程中在细胞上差异表达。我们发现缺乏HSA的前B细胞（由于两个等位基因的靶向破坏）仍然可以通过VLA- 4与肿瘤坏死因子α刺激的内皮瘤细胞结合。然而，这种结合不能被抗VCAM-1抗体阻断。HSA表达的恢复恢复了可复制的VCAM-1结合。我们还发现，缺乏HSA的前B细胞不与纤连蛋白的FN 40片段结合，但HSA的再表达恢复了VLA-4介导的与纤连蛋白的结合。因此，HSA在前B细胞上的表达改变了VLA-4对两种已知配体的结合特异性。
The integrin very late antigen, (VLA-4) alpha 4 beta 1 and its counter receptor vascular cell adhesion molecule 1 (VCAM-1) are involved in B cell maturation and pre-B cell attachment to bone marrow stroma cells. We have analyzed whether heat-stable antigen (HSA), a marker for immature leukocytes, is involved in such cell adhesion phenomena. HSA is a glycolipid-anchored, highly glycosylated surface protein differentially expressed on cells during the maturation of both the hematopoietic and nervous systems. We found that pre-B cells lacking HSA (due to targeted disruption of both alleles) can still bind via VLA- 4 to tumor necrosis factor alpha-stimulated endothelioma cells. This binding, however, cannot be blocked by an anti-VCAM-1 antibody. Restoration of HSA expression restores the inhibitable VCAM-1 binding. We also found that pre-B cells lacking HSA did not bind to the FN40 fragment of fibronectin but reexpression of HSA restored VLA-4-mediated binding to fibronectin. Thus, expression of HSA on pre-B cells modifies the binding specificity of VLA-4 for two known ligands.