Lymphocyte function-associated antigen 1 dominates very late antigen 4 in binding of activated T cells to endothelium

Y van Kooyk, E van de Wiel-van Kemenade, P Weder, R J Huijbens, C G Figdor

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Lymphocyte function-associated antigen 1/intercellular adhesion molecule 1 (LFA-1/ICAM-1)-and very late antigen 4/vascular cell adhesion molecule 1 (VLA-4/VCAM-1)-mediated adhesion of T lymphocytes to endothelial cells (EC) can be regulated by increased expression of ICAM-1 and VCAM-1 upon cytokine treatment of EC, or by activation of the integrin molecules LFA-1 and VLA-4 on T cells. Here, we provide evidence that preferential usage of LFA-1 over VLA-4 is yet another mechanism to control T cell adhesion. We observed that binding of activated T lymphocytes, as opposed to resting T cells, to EC is essentially mediated through LFA-1 and not through VLA-4. VLA-4-mediated adhesion of T cells to EC is only found when LFA-1 is not expressed or not functional, as observed for several T cell leukemia cell lines. These results suggest that LFA-1-mediated adhesion dominates and may downregulate VLA-4-mediated adhesion through an unidentified mechanism.

Original languageEnglish
Pages (from-to)185-90
Number of pages6
JournalJournal of Experimental Medicine
Volume177
Issue number1
Publication statusPublished - 1 Jan 1993

Cite this

van Kooyk, Y ; van de Wiel-van Kemenade, E ; Weder, P ; Huijbens, R J ; Figdor, C G. / Lymphocyte function-associated antigen 1 dominates very late antigen 4 in binding of activated T cells to endothelium. In: Journal of Experimental Medicine. 1993 ; Vol. 177, No. 1. pp. 185-90.
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title = "Lymphocyte function-associated antigen 1 dominates very late antigen 4 in binding of activated T cells to endothelium",
abstract = "Lymphocyte function-associated antigen 1/intercellular adhesion molecule 1 (LFA-1/ICAM-1)-and very late antigen 4/vascular cell adhesion molecule 1 (VLA-4/VCAM-1)-mediated adhesion of T lymphocytes to endothelial cells (EC) can be regulated by increased expression of ICAM-1 and VCAM-1 upon cytokine treatment of EC, or by activation of the integrin molecules LFA-1 and VLA-4 on T cells. Here, we provide evidence that preferential usage of LFA-1 over VLA-4 is yet another mechanism to control T cell adhesion. We observed that binding of activated T lymphocytes, as opposed to resting T cells, to EC is essentially mediated through LFA-1 and not through VLA-4. VLA-4-mediated adhesion of T cells to EC is only found when LFA-1 is not expressed or not functional, as observed for several T cell leukemia cell lines. These results suggest that LFA-1-mediated adhesion dominates and may downregulate VLA-4-mediated adhesion through an unidentified mechanism.",
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author = "{van Kooyk}, Y and {van de Wiel-van Kemenade}, E and P Weder and Huijbens, {R J} and Figdor, {C G}",
year = "1993",
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Lymphocyte function-associated antigen 1 dominates very late antigen 4 in binding of activated T cells to endothelium. / van Kooyk, Y; van de Wiel-van Kemenade, E; Weder, P; Huijbens, R J; Figdor, C G.

In: Journal of Experimental Medicine, Vol. 177, No. 1, 01.01.1993, p. 185-90.

Research output: Contribution to journalArticleAcademicpeer-review

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T1 - Lymphocyte function-associated antigen 1 dominates very late antigen 4 in binding of activated T cells to endothelium

AU - van Kooyk, Y

AU - van de Wiel-van Kemenade, E

AU - Weder, P

AU - Huijbens, R J

AU - Figdor, C G

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N2 - Lymphocyte function-associated antigen 1/intercellular adhesion molecule 1 (LFA-1/ICAM-1)-and very late antigen 4/vascular cell adhesion molecule 1 (VLA-4/VCAM-1)-mediated adhesion of T lymphocytes to endothelial cells (EC) can be regulated by increased expression of ICAM-1 and VCAM-1 upon cytokine treatment of EC, or by activation of the integrin molecules LFA-1 and VLA-4 on T cells. Here, we provide evidence that preferential usage of LFA-1 over VLA-4 is yet another mechanism to control T cell adhesion. We observed that binding of activated T lymphocytes, as opposed to resting T cells, to EC is essentially mediated through LFA-1 and not through VLA-4. VLA-4-mediated adhesion of T cells to EC is only found when LFA-1 is not expressed or not functional, as observed for several T cell leukemia cell lines. These results suggest that LFA-1-mediated adhesion dominates and may downregulate VLA-4-mediated adhesion through an unidentified mechanism.

AB - Lymphocyte function-associated antigen 1/intercellular adhesion molecule 1 (LFA-1/ICAM-1)-and very late antigen 4/vascular cell adhesion molecule 1 (VLA-4/VCAM-1)-mediated adhesion of T lymphocytes to endothelial cells (EC) can be regulated by increased expression of ICAM-1 and VCAM-1 upon cytokine treatment of EC, or by activation of the integrin molecules LFA-1 and VLA-4 on T cells. Here, we provide evidence that preferential usage of LFA-1 over VLA-4 is yet another mechanism to control T cell adhesion. We observed that binding of activated T lymphocytes, as opposed to resting T cells, to EC is essentially mediated through LFA-1 and not through VLA-4. VLA-4-mediated adhesion of T cells to EC is only found when LFA-1 is not expressed or not functional, as observed for several T cell leukemia cell lines. These results suggest that LFA-1-mediated adhesion dominates and may downregulate VLA-4-mediated adhesion through an unidentified mechanism.

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KW - Intercellular Adhesion Molecule-1

KW - Lymphocyte Activation

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KW - Mice

KW - Receptors, Very Late Antigen/physiology

KW - T-Lymphocytes/physiology

KW - Vascular Cell Adhesion Molecule-1

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JO - Journal of Experimental Medicine

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