Endothelial-Leukocyte Adhesion Molecules in Human Disease

Bevilacqua, Michael P.; Nelson, Richard M.; Mannori, Gianna; Cecconi, Oliviero

doi:10.1146/annurev.med.45.1.361

Cited by 402 publications

(46 citation statements)

References 97 publications

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“…Activated T lymphocytes are central to the pathogenesis of a large number of immunologically mediated inflammatory diseases [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12]. Whether causing diseases or participating in a normal adaptive immune response, memory T cells must efficiently exit the bloodstream at the appropriate sites in peripheral tissue.…”

Section: Introductionmentioning

confidence: 99%

“…Typically, fewer than 20% of circulating peripheral blood T cells are CLA–positive. In contrast, more than 85% if not all of skin–infiltrating T cells express this E–selectin binding molecule, implicating CLA as an important cell surface adhesion molecule involved in homing of T lymphocytes to the skin [2, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 18, 19, 20, 21]. …”

Section: Introductionmentioning

confidence: 99%

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Functional Cutaneous Lymphocyte Antigen Can Be Induced in Essentially All Peripheral Blood T Lymphocytes

Armerding

Kupper²

1999

Int Arch Allergy Immunol

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The cutaneous lymphocyte–associated antigen (CLA) is a skin–homing receptor expressed on a minority of memory–type peripheral blood T (PBT) lymphocytes. Induction of high–level CLA expression in PBT has previously been difficult to accomplish in vitro. Here we report that constitutive CLA expression could be readily induced in virtually all PBT by various polyclonal activators. There was no requirement for accessory cells or addition of other mediators except for IL–2 for maintaining cell survival. Absence of serum in the culture medium was important for optimal induction of CLA. The number of T cells adhering to E–selectin as well as tethering and shear stress resistance under hydrodynamic flow increased in correlation with the level of cell surface CLA expressed. Clonal analysis of CLA induction revealed that in serum–containing medium, which permits the majority of T cells to expand, only a minority of clones did not express CLA. Such T cells could be induced to highly express CLA within 8 days by switching from serum–containing to serum–free medium. This cell–surface phenotype change was closely associated with acquisition of E–selectin ligand activity. Fucosyltransferase VII, which is believed to be important for the generation of the CLA epitope on the P–selectin glycoprotein ligand–1 (PSGL–1) backbone, was shown to be significantly increased in CLA–positive versus CLA–negative T cell populations by PCR analysis. Our findings are consistent with the idea that restriction of CLA expression after activation, rather than positive selection of predetermined T cell subpopulations exposed to restrictive stimulatory conditions in unique microenvironments, may be important in vivo.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Functional Cutaneous Lymphocyte Antigen Can Be Induced in Essentially All Peripheral Blood T Lymphocytes

Armerding

Kupper²

1999

Int Arch Allergy Immunol

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“…Inhibition of leukocyte rolling or leukocyte sticking to the venular wall interrupts this sequence and prevents subsequent migration of the activated leukocytes and therefore injury [24, 25]. …”

Section: Discussionmentioning

confidence: 99%

Leukocyte Sequestration in Pulmonary Microvessels and Lung Injury following Systemic Complement Activation in Rabbits

Kuhnle¹,

Kiefmann²,

Sckell³

et al. 1999

J Vasc Res

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Inflammatory reactions are associated with sequestration of leukocytes in the lung. Complement activation leads to accumulation of leukocytes in alveolar septa and alveoli, to lung edema and hemorrhage. Although in organs other than the lung leukocytes interact with the vascular endothelium only in postcapillary venules, alveolar capillaries are considered to be the site of leukocyte sequestration in the lung. However, pulmonary venules and arterioles have not been investigated systematically after complement activation so far. A closed thoracic window was implanted in anesthetized rabbits; leukocytes and red blood cells were stained, and the movement of these cells was measured in superficial pulmonary arterioles, venules and alveolar capillaries using fluorescence video microscopy before and 30 and 60 min after infusion of cobra venom factor (CVF). Erythrocyte velocity and macrohemodynamic conditions did not change after CVF infusion and were not different from the sham-treated controls. The number of sticking leukocytes increased significantly compared to baseline and control: by 150% in arterioles and in venules and by 740% in alveolar capillaries within 60 min after CVF infusion. The width of alveolar septa in vivo was significantly enlarged after CVF infusion, indicating interstitial pulmonary edema. At the end of the experiments, myeloperoxidase activity was higher in the CVF group, showing leukocyte sequestration in the whole organ. It is concluded that complement activation by CVF induces leukocyte sequestration in lung arterioles, venules and alveolar capillaries and leads to mild lung injury.

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“…Elevated expression of ICAM-1 has been demonstrated in a variety of inflammatory/immune system mediated human diseases [33], e.g., rheumatoid arthritis, psoriasis, ulcerative colitis, asthma, allograft rejection, and has been shown often to correlate with leukocyte infiltration in the diseased tissue [34]. Regulation of ICAM-1 expression occurs in a cell-specific way and depends on availability of specific receptors for extracellular signals, activity of signal transduction pathways, and availability of required transcription factors [35].…”

Section: Icam-1 and Reperfusion Injurymentioning

confidence: 99%

Diapedesis of Leukocytes: Antisense Oligonucleotides for Rescue

Dragun

Haller²

1999

Nephron Exp Nephrol

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Ischemia-reperfusion injury is an acute inflammatory process during which leukocytes are intimately involved. In this review, we summarize the current data on the leukocyte cell adhesion cascade in ischemia-reperfusion injury, focus upon studies which have demonstrated specific cell adhesion molecule interactions which mediate the leukocyte involvement in ischemia-reperfusion injury, and suggest future avenues of therapeutic interventions. The increased adhesion between activated vascular endothelium and peripheral blood leukocytes is central to the structural and the functional impairment in ischemia-reperfusion injury. Several families of adhesion molecules, namely the selectins, the intercellular adhesion molecules (ICAMs), and the integrins expressed either on the endothelium or on the leukocytes, are involved the cascade of events. Sequential and overlapping cellular interactions between the members of the three gene families of adhesion receptors result in adhesion of the leukocytes to the endothelium and extravasation at the site of ischemia. The functional importance of ICAM-1 and its β₂ integrin ligands in ischemia-reperfusion of the kidney has been demonstrated by monoclonal antibody blockade studies, in knockout mice and by treatment with antisense oligodeoxynulceotides (ODN). We have shown that antisense ODN for ICAM-1 protected the kidney against ischemic renal failure. In addition, in transplanted kidneys, ICAM-1 inhibition by antisense ODN ameliorates ischemia-reperfusion injury and prevents delayed graft function. Recent developments in antisense ODN technology make this a promising therapeutic approach, and antisense ODN treatment of donors or donor organs for ICAM-1 may be useful for the prevention of reperfusion injury in human renal transplantation and could influence acute and chronic graft function.

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Endothelial-Leukocyte Adhesion Molecules in Human Disease

Cited by 402 publications

References 97 publications

Functional Cutaneous Lymphocyte Antigen Can Be Induced in Essentially All Peripheral Blood T Lymphocytes

Functional Cutaneous Lymphocyte Antigen Can Be Induced in Essentially All Peripheral Blood T Lymphocytes

Leukocyte Sequestration in Pulmonary Microvessels and Lung Injury following Systemic Complement Activation in Rabbits

Diapedesis of Leukocytes: Antisense Oligonucleotides for Rescue

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