Intracellular domain of brain endothelial intercellular adhesion molecule-1 is essential for T lymphocyte-mediated signaling and migration.
Intracellular domain of brain endothelial intercellular adhesion molecule-1 is essential for T lymphocyte-mediated signaling and migration.
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DOI：
10.4049/jimmunol.171.4.2099
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发表时间：
2003-08-15
期刊：
影响因子：
--
通讯作者：
Adamson P
中科院分区：
文献类型：
--
作者：
Greenwood J;Amos CL;Walters CE;Couraud PO;Lyck R;Engelhardt B;Adamson P
In order to examine the role of the ICAM-1 C-terminal domain in mediating transendothelial T-lymphocyte migration and ICAM-1 mediated signal transduction. Mutant human ICAM-1 molecules were expressed in rat brain microvascular endothelial cells. Expression of human wild type ICAM-1 in rat brain endothelial cells (EC) resulted in a significant increase over basal levels in both adhesion and transendothelial migration of rat T-lymphocytes. EC expressing ICAM-1, in which the conserved tyrosine residue at codon 512 was substituted with phenylalanine (hICAM-1Y512F), also exhibited increased lymphocyte migration albeit less than with wild type ICAM-1. Conversely, expression of truncated human ICAM-1 proteins, in which either the intracellular domain was deleted (hICAM-1ΔC) or both the intracellular and transmembrane domains were deleted through construction of a glycophospholipid anchor (GPI-hICAM-1), did not result in an increase in lymphocyte adhesion and their ability to increase transendothelial migration was attenuated. Truncated ICAM-1 proteins were also unable to induce ICAM-1 mediated Rho GTPase activation. Rat EC treated with cell permeant penetratin-ICAM-1 peptides comprising human or rat ICAM-1 intracellular domain sequences inhibited transendothelial lymphocyte migration but not adhesion. Peptides containing a phosphotyrosine residue were equally potent at inhibiting lymphocyte migration. These data demonstrate that the intracellular domain of ICAM-1 is essential for transendothelial migration of lymphocytes, and that peptidomimetics of the ICAM-1 intracellular domain can also inhibit this process. Such competitive inhibition of transendothelial lymphocyte migration, in the absence of an affect on adhesion, further implicates ICAM-1-mediated signalling events in the facilitation of T-lymphocyte migration across brain EC. Thus agents which mimic the ICAM-1 intracellular domain may be attractive targets for novel anti-inflammatory therapeutics.
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DOI：
10.1083/jcb.143.5.1385
发表时间：
1998-11-30
期刊：
The Journal of cell biology
影响因子：
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作者：
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通讯作者：
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DOI：
10.1083/jcb.200112126
发表时间：
2002-06-24
期刊：
The Journal of cell biology
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通讯作者：
Sanchez-Madrid F
影响因子：
4.4
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通讯作者：
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发表时间：
1997-08-25
期刊：
The Journal of cell biology
影响因子：
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作者：
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通讯作者：
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DOI：
10.1111/j.1432-1033.1996.0173q.x
发表时间：
1996-05-01
期刊：
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影响因子：
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作者：
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通讯作者：
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