Four molecular pathways of T cell adhesion to endothelial cells: roles of LFA-1, VCAM-1, and ELAM-1 and changes in pathway hierarchy under different activation conditions.

Shimizu, Yoji; Newman, Walter; Gopal, T V; Horgan, Kevin J.; Graber, Norma L.; Beall, L D; Seventer, Gijs A. van; Shaw, Stephen

doi:10.1083/jcb.113.5.1203

Cited by 324 publications

(163 citation statements)

References 52 publications

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“…1 B), A23187, CD7, and CD28 crosslinking also increase adhesion to the VLA-4 ligand VCAM-1 (Fig. I A), extending our earlier findings on VCAM-1 adhesion using PMA activation (21,23). These results suggest that these activation signals act coordinately on multiple T cell integrins, enabling T cells to adhere to a variety of cell surface and ECM ligands, mAb blocking studies demonstrated that adhesion to these ligands after activation occurs via the expected integrin receptors (data not shown).…”

Section: Multiple Activation Signals Upregulate T Cell Adhesion To Vcsupporting

confidence: 77%

Crosslinking of the T cell-specific accessory molecules CD7 and CD28 modulates T cell adhesion.

Shimizu

Seventer

Ennis

et al. 1992

The Journal of Experimental Medicine

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176

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SummaryRegulated adhesion enables T cells to migrate through tissue and transiently interact with an endless succession of cells. Monoclonal antibody (mAb) engagement of the CD3/T cell receptor (TCR) complex results in a rapid and transient augmentation of the adhesion function of LFA-1 and VLA integrin molecules on human T cells. We show in this study that mAb crosslinking of the T cell-specific accessory molecules CD7 and CD28, or treatment with the Ca 2+ ionophore A23187, results in the rapid induction of integrin-mediated adhesion to three distinct ligands: the extracellular matrix protein fibronectin, and the cell surface molecules ICAM-1 and VCAM-1. Like CD3 crosslinking, increased adhesion via CD7 and CD28 crosslinking appears to involve both protein kinase C (PKC) and cAMP-dependent protein kinases. In contrast, A23187 induction of adhesion is unaffected by PKC inhibitors. CD7 is preferentially expressed on naive T cells and is unique in being a potent inducer of naive T cell adhesion. Enhanced expression/function of adhesion-inducing molecules thus overcomes relative deficits in adhesion receptor expression."[ mphocytes express a multitude of cell surface receptors .1_r that are capable of mediating adhesion to other cells and proteins (1, 2). Regulation of the functional activity of these adhesion molecules is critical to both T cell migration and recognition, since T cells must transiently interact with cells and proteins found in the extracellular environment. One important element in the regulation of adhesion is the rapid increase in the adhesive function of integrin molecules that occurs after crosslinking of the CD3/TCR complex by mAb (3-6) or foreign antigen (7). Integrins mediate T cell adhesion to other cells via interactions such as LFA-1 binding to its ligands ICAM-1 and ICAM-2, and VLA-4 binding to VCAM-1, and also to extraceUular matrix (ECM) 1 components via interactions such as VLA-4 and VLA-5 to fibronectin (FN) (1, 2, 8). Activation of other lymphoid cell types by mAb crosslinking of functionally relevant cell surface molecules also results in increased LFA-l-dependent adhesion. Such molecules include HLA class II (9) and CD14 (10) on monocytes, and surface immunoglobulin (11), CD19 (12), and CD40 (13) We reasoned that the functional activity of integrin molecules on human T cells might also be increased by mAb crosslinking of other molecules besides the CD3/TCR. In this study we report the ability of three different activation signals to increase integrin-mediated adhesion: the Ca 2 + ionophore A23187, and mAb crosslinking of the CD7 and CD28 molecules, both of which have been implicated as T cell activation molecules (14-16). These activation signals can coordinately increase T cell adhesion to three different ligands: the LFA-1 ligand ICAM-1, the VLA-4 endothelial cell surface ligand VCAM-1, and the VLA-4 and VLA-5 ligand FN. We demonstrate similarities in the biochemical signals generated by CD3, CDT, and CD28 crosslinking that distinguish receptor-mediated activation from the eff...

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Section: Multiple Activation Signals Upregulate T Cell Adhesion To Vcsupporting

confidence: 77%

Crosslinking of the T cell-specific accessory molecules CD7 and CD28 modulates T cell adhesion.

Shimizu

Seventer

Ennis

et al. 1992

The Journal of Experimental Medicine

Self Cite

176

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“…Early investigations of leukocyte adhesion settled leukocytes onto endothelial monolayers or tissue sections 26,27 in the absence of shear stress, which failed to mimic the interactions that occur in blood flow. Recent studies confirm that shear stress is a critical factor that determines whether leukocyte-endothelial interactions occur, making it important to conduct analyses under physiological levels of shear stress.…”

Section: Discussionmentioning

confidence: 99%

Lymphocyte traffic through sinusoidal endothelial cells is regulated by hepatocytes

et al. 2005

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Crosstalk between hepatic sinusoidal ECs and closely juxtaposed hepatocytes via vascular endothelial growth factor is essential for the maintenance of sinusoidal endothelial growth and differentiation. We propose that paracrine interactions between endothelial cells and hepatocytes also may be responsible for the unique complement of adhesion receptors expressed on sinusoidal endothelium that regulate the recruitment of lymphocytes into the liver. To address this hypothesis, we developed an in vitro model of the hepatic sinusoid in which flowing lymphocytes could interact with hepatic endothelium conditioned by the presence of hepatocytes. Human hepatic sinusoidal endothelial cells cocultured with hepatocytes were activated so that they supported the adhesion of lymphocytes at levels equivalent to those seen on endothelium stimulated with the inflammatory cytokine tumour necrosis factor-␤.

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“…In vitro binding assay using cytokine-activated endothelial cells has demonstrated that multiple adhesive interactions with E-selectin, VCAM-1, ICAM-1, and L-selectin are required for adhesion and extravasation of T cells 6,7,26 ; E-selectin mediates initial, low-affinity adhesion 44 and ICAM-I mediates secondary, high-affinity adhesion, and VCAM-1 is involved in both initial and secondary adhesion. 28 Among adhesion molecules, E-selectin and VCAM-1 are considered to be more important for lymphocyte adhesion because they appeared at 4 to 6 hours after Con A injection before the manifestation of lymphocyte …”

Section: Discussionmentioning

confidence: 99%

“…6 Among them, E-selectin, P-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular endothelial cell adhesion molecule-1 (VCAM-1) play critical roles in T-cells rolling over and sticking to endothelial cells. 6,7,26,27,28 Clinical studies also showed that E-selectin and VCAM-1, which were absent in normal human liver tissues, came to strongly express in inflammatory liver diseases. 29 In Con A-induced murine hepatitis as well, we observed VCAM-1 expression in the hepatic vasculature at the time of lymphocyte infiltration, 18 suggesting its role in the entrapment of circulating lymphocytes during inflammation.…”

mentioning

confidence: 99%

Sublobular veins as the main site of lymphocyte adhesion/transmigration and adhesion molecule expression in the porto-sinusoidal-hepatic venous system during concanavalin A-induced hepatitis in mice

et al. 2000

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Lymphocyte infiltration is a manifest feature of hepatitis. To reveal the main site and mechanism of lymphocyte adhesion/extravasation in the hepatic vasculature during inflammation, we morphometrically and histologically analyzed these events in relation to adhesion molecule expression using a murine model of T-cell mediated hepatitis induced by concanavalin A (Con A). Although lymphocyte adhesion was restricted to the sinusoids in untreated mice, it increased in all the segments of porto-sinusoidal-hepatic venous system 8 hours after Con A injection; the number of adhering lymphocytes per unit vascular circumference was the largest in the sublobular veins, relatively large in the central veins and small hepatic veins, and relatively small in the sinusoids and negligible in the portal veins. At 20 hours, extravascular lymphocytes showed similar distribution to lymphocyte adhesion at 8 hours except in the portal veins, around which they were possibly accumulated by the translocation of extrasinusoidal lymphocytes. E-selectin and vascular cell adhesion molecule-1 (VCAM-1) were transiently expressed at 4 to 6 hours, whereas P-selectin and intercellular adhesion molecule-1 were not changed between 0 and 48 hours. In particular, E-selectin expression coincided with that of lymphocyte adhesion in distribution.

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Four molecular pathways of T cell adhesion to endothelial cells: roles of LFA-1, VCAM-1, and ELAM-1 and changes in pathway hierarchy under different activation conditions.

Cited by 324 publications

References 52 publications

Crosslinking of the T cell-specific accessory molecules CD7 and CD28 modulates T cell adhesion.

Crosslinking of the T cell-specific accessory molecules CD7 and CD28 modulates T cell adhesion.

Lymphocyte traffic through sinusoidal endothelial cells is regulated by hepatocytes

Sublobular veins as the main site of lymphocyte adhesion/transmigration and adhesion molecule expression in the porto-sinusoidal-hepatic venous system during concanavalin A-induced hepatitis in mice

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