DISTINCT BINDING OF T-LYMPHOCYTES TO ICAM-1, ICAM-2 OR ICAM-3 UPON ACTIVATION OF LFA-1
DISTINCT BINDING OF T-LYMPHOCYTES TO ICAM-1, ICAM-2 OR ICAM-3 UPON ACTIVATION OF LFA-1
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DOI：
10.1002/eji.1830240933
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发表时间：
1994-09-01
影响因子：
5.4
通讯作者：
FIGDOR, CG
中科院分区：
文献类型：
--
作者：
BINNERTS, ME;VANKOOYK, Y;FIGDOR, CG
LFA-1(CD11a/CD18)通过与其配体之一ICAM-1、ICAM-2或ICAM-3结合来介导白细胞黏附。在这里，我们研究了已知的诱导ICAM-1黏附的刺激是否也能诱导LFA-1介导的T淋巴细胞与ICAM-2和ICAM-3转染体的黏附。我们观察到佛波酯、Mn2+、CD3的交联或激活抗LfA-1抗体能增强LFA-L介导的T细胞与ICAM-2和ICAM-3的黏附，但幅度小于ICAM-1。这些结果表明，与已报道的与ICAM-1的黏附相似，LFA-1的激活也是与ICAM-2和-3黏附所必需的。此外，结果提示ICAM-1是活化T淋巴细胞表面LFA-1的主要配体。有趣的是，我们观察到，与激活抗CD18抗体相比，激活抗CD11a抗体不能诱导LFA-1与所有三种配体的黏附。抗体MEM-83促进与ICAM-1的结合，同时抑制LFA-1与ICAM-2和ICAM-3的相互作用。抗体NKI-L16选择性地诱导与ICAM-1和ICAM-2的黏附，但不能诱导与ICAM-3的黏附。我们的结果表明，LFA-1的不同构象需要支持与ICAM-2、-2或-3的黏附，并且配体可能结合在LFA-1分子的不同位置。
LFA-1 (CD11a/CD18) mediates leukocyte adhesion by binding to one of its ligands: ICAM-1, ICAM-2 or ICAM-3. Here, we investigated whether stimuli known to induce adhesion to ICAM-1 were also capable of inducing LFA-1-mediated adhesion of T lymphocytes to ICAM-2 and -3 transfectants. We observed that phorbol 12-myristate 13-acetate, Mn2+, cross-linking of CD3 or activating antibodies against LFA-1 enhanced LFA-l-mediated T cell adhesion to ICAM-2 and -3, although to a lesser extent than to ICAM-1. These results indicate that, similar to what has been reported for adhesion to ICAM-1, activation of LFA-1 is also required for adhesion to ICAM-2 and -3. Furthermore, the results suggest that ICAM-1 is the major ligand for LFA-1 on activated T lymphocytes. Interestingly, we observed that in contrast to activating antibodies against CD18, activating antibodies against CD11a were incapable of inducing adhesion of LFA-1 to all three ligands. The antibody MEM-83 stimulated binding to ICAM-1, while at the same time inhibiting the interaction of LFA-1 with ICAM-2 and -3. The antibody NKI-L16 selectively induced adhesion to ICAM-1 and -2, but not to ICAM-3. Our results suggest that different conformations of LFA-1 are required to support adhesion to ICAM-2, -2 or -3, and that ligands may bind on different sites of the LFA-1 molecule.