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Blood, 15 November 2003, Vol. 102, No. 10, pp. 3675-3683.
Prepublished online as a Blood First Edition Paper on July 31, 2003; DOI 10.1182/blood-2003-02-0358.
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IMMUNOBIOLOGY
T-cell interaction with ICAM-1/ICAM-2 double-deficient brain endothelium in vitro: the cytoplasmic tail of endothelial ICAM-1 is necessary for transendothelial migration of T cells
Ruth Lyck,
Yvonne Reiss,
Nicole Gerwin,
John Greenwood,
Peter Adamson, and
Britta Engelhardt
From the Max-Planck Institute for Physiological and Clinical Research, W G Kerckhoff Institute, Bad Nauheim, Germany; Max-Planck-Institute for Vascular Cell Biology, Münster, Germany; Millenium Pharmaceuticals, Cambridge, MA; and the Institute of Ophthalmology, London, United Kingdom.
Endothelial intercellular adhesion molecule 1 (ICAM-1) and ICAM-2 are both involved in lymphocyte extravasation during immunosurveillance and inflammation. To define their exact role during T-cell extravasation, we used mouse T cells and ICAM-1-/-ICAM-2-/- brain endothelioma cells. ICAM-1-/-ICAM-2-/- brain endothelioma cells did not support transendothelial migration (TEM) of T cells in vitro. Re-expression of different ICAM-1 mutants in the ICAM-1-/-ICAM-2-/- endothelioma line bEndI1/2.1 or in the ICAM-1-/- endothelioma line bEndI1.1 demonstrated that the extracellular domain of ICAM-1 suffices to support T-cell adhesion while the presence of the cytoplasmic tail was strictly required for TEM. Surprisingly, tyrosine phosphorylation of endothelial ICAM-1 was not necessary for TEM of T cells or for Rho guanosine triphosphatase (RhoGTPase) activation. Furthermore, cytoplasmic deletion mutants of ICAM-1 were unable to mediate RhoGTPase activation. Thus, our data demonstrate that the cytoplasmic tail of endothelial ICAM-1—independently from tyrosine phosphorylation—is essential for supporting TEM of T lymphocytes, while Rho signaling is involved in endothelial cells. (Blood. 2003;102:3675-3683)
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