Expression of the human leukocyte adhesion molecule, LAM1. Identity with the TQ1 and Leu-8 differentiation antigens.
Expression of the human leukocyte adhesion molecule, LAM1. Identity with the TQ1 and Leu-8 differentiation antigens.
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DOI：
10.4049/jimmunol.144.2.532
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发表时间：
1990-01
影响因子：
4.4
通讯作者：
T. Tedder;Ann C. Penta;H. Levine;A. Freedman
中科院分区：
文献类型：
--
作者：
T. Tedder;Ann C. Penta;H. Levine;A. Freedman
LAM1分子是细胞粘附/归巢分子新家族的一员，在其氨基末端包含一个凝集素样结构域，随后是一个表皮生长因子样结构域和短一致重复单元，如在C3/C4结合蛋白中发现的。制备了两种与白细胞粘附分子1 （LAM1）反应的单抗，用于检测LAM1在细胞表面的表达。抗lam1抗体与大多数血液淋巴细胞、NK细胞、中性粒细胞和单核细胞反应。LAM1也在表型未成熟和成熟胸腺细胞亚群中表达。在PMA暴露的60分钟内，血液淋巴细胞从细胞表面快速调节LAM1。随着LAM1从细胞表面的丢失，pma处理的淋巴细胞失去了与淋巴结高内皮小静脉结合的能力，这表明LAM1的表达可能在淋巴细胞归巢中起作用。有丝分裂原刺激血液T淋巴细胞和B淋巴细胞也导致LAM1表达下降，但下降速度较慢。LAM1仅在少数脾淋巴细胞中弱表达。然而，在培养基中单独培养脾脏淋巴细胞会导致一部分细胞（40%至60%）LAM1的表达增加。同时刺激脾淋巴细胞的有丝分裂原，最初导致LAM1表达下调，随后LAM1表达升高，随后LAM1从细胞表面消失。抗LAM1抗体的反应模式与报道的TQ1和Leu-8抗体相同，并且这些抗体都与转染了LAM1 cDNA的细胞反应。因此，LAM1在白细胞中广泛表达，LAM1的结合可能参与白细胞外渗到淋巴器官或急性炎症部位的过程，随后LAM1从细胞表面丢失。
The LAM1 molecule is a member of the new family of cellular adhesion/homing molecules that contain a lectin-like domain at their amino-terminal end followed by an epidermal growth factor-like domain and short consensus repeat units like those found in C3/C4 binding proteins. Two mAb that react with the leukocyte adhesion molecule 1 (LAM1) were produced and used to examine the cell-surface expression of LAM1. The anti-LAM1 antibodies were reactive with the majority of blood lymphocytes, NK cells, neutrophils, and monocytes. LAM1 was also expressed by subpopulations of phenotypically immature and mature thymocytes. Blood lymphocytes rapidly modulated LAM1 from the cell surface during PMA exposure for 60 min. Coordinate with the loss of LAM1 from the cell surface, PMA-treated lymphocytes lost the ability to bind to lymph node high endothelial venules, indicating that expression of LAM1 may play a role in lymphocyte homing. Mitogen stimulation of blood T and B lymphocytes also resulted in decreased LAM1 expression, but at a slower rate. LAM1 was only weakly expressed by a minority of spleen lymphocytes. However, culturing spleen lymphocytes in media alone resulted in increased expression of LAM1 by a subpopulation of the cells (40 to 60%). Concomitant mitogen stimulation of spleen lymphocytes resulted initially in down-regulation of LAM1 expression followed by increased expression of LAM1 and then subsequent loss of LAM1 from the cell surface. The pattern of anti-LAM1 antibody reactivity was identical to that reported for the TQ1 and Leu-8 antibodies, and all of these antibodies reacted with cells transfected with the LAM1 cDNA. Thus, LAM1 is broadly expressed by leukocytes, and binding of LAM1 may participate in the process of leukocyte extravasation into lymphoid organs or sites of acute inflammation with subsequent loss of LAM1 from the cell surface.