E-selectin and vascular cell adhesion molecule-1 are critical for initial trafficking of helper-inducer/memory T cells in psoriatic plaques

Wakita, H.

doi:10.1001/archderm.130.4.457

Cited by 19 publications

(12 citation statements)

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“…The time-dependent induction of VCAM-1, E-selectin, and ICAM-1 by a number of proinflammatory signals represents a common feature of cutaneous inflammatory disorders. Specifically, VCAM-1 and E-selectin are viewed as important participants relevant to the pathogenesis of psoriasis by allowing initial trafficking of memory T-lymphocytes into psoriatic lesions (25). Therefore, the modulation and inhibition of CAM expression on EC and leukocytes may represent a potential target of retinoid action at sites of inflammation, particularly those characterized by mononuclear infiltrates.…”

Section: Discussionmentioning

confidence: 99%

Retinoic acid inhibits the regulated expression of vascular cell adhesion molecule-1 by cultured dermal microvascular endothelial cells.

Gille¹,

Paxton²,

Lawley³

et al. 1997

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

Retinoic acid inhibits the regulated expression of vascular cell adhesion molecule-1 by cultured dermal microvascular endothelial cells.

Gille¹,

Paxton²,

Lawley³

et al. 1997

J. Clin. Invest.

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“…Two good candidates for such a role are VCAM-1 and ICAM-I , which are widely expressed in tissues in various autoimmune, inflammatory, and allergic conditions, including rheumatoid arthritis (4,12,13), psoriasis (28,29), and asthma (30). Previous studies have suggested an important role for VCAM-1 and ICAM-1 in lymphocyte adhesion to synovial fibroblasts (4,22).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of lymphocyte adhesion to cytokine‐activated synovial fibroblasts by glucocorticoids involves the attenuation of vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 gene expression

Tessier

Cattaruzzi

McColl

1996

Arthritis & Rheumatism

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Objective. The aim of this study was to evaluate the ability of glucocorticoids to inhibit lymphocyte adhesion to human synovial fibroblasts. Methods. Adhesion of lymphocytes to cultured synovial fibroblasts was measured by counting the number of cells bound to fibroblasts. Surface expression of intercellular adhesion molecule 1 (ICAM‐1) was measured by enzyme‐linked immunosorbent assay, while vascular cell adhesion molecule 1 (VCAM‐1) surface expression was measured by flow cytometry. ICAM‐1 and VCAM‐1 messenger RNA (mRNA) levels were assessed by Northern blot analysis. Results. Stimulation of synovial fibroblasts by the proinflammatory cytokines tumor necrosis factor α, interleukin‐1β, and interferon‐γ resulted in a dose‐dependent increase in lymphocyte adhesion to synovial fibroblasts. This response was inhibited by preincubation of the cells with the synthetic glucocorticoid dexa‐methasone. Since lymphocyte adhesion to synovial fibroblasts is known to be mediated by VCAM‐1 and ICAM‐1, we examined the modulation of VCAM‐1 and ICAM‐1 expression in these cells. All 3 cytokines stimulated VCAM‐1 and ICAM‐1 surface and mRNA expression. Dexamethasone inhibited both VCAM‐1 and ICAM‐1 surface and mRNA expression in a dose‐dependent manner, which correlated with the inhibition of lymphocyte adhesion. Conclusion. Taken together, these results suggest that glucocorticoids may reduce inflammatory responses at extravascular sites by inhibiting the expression of these adhesion molecules, thereby reducing the adhesion of lymphocytes to connective tissue cells.

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“…Due to its crucial role in the transmigration of specific myeloid populations to sites of inflammation, the selectin/selectin–ligand axis is involved in the development of many acute and chronic inflammatory conditions ( 181 , 182 ). In fact, cutaneous inflammatory disorders, such as allergic contact dermatitis ( 183 ), atopic dermatitis ( 184 – 188 ), and psoriasis ( 183 , 184 , 189 – 191 ), are known to be promoted by the upregulation of selectins on dermal microvasculature. Specifically, P- and E-selectins are upregulated in skin lesions of cutaneous inflammatory patients, which enables inflammatory mononuclear phagocyte infiltration with subsequent release of soluble cytotoxic mediators, T cell activation, and destruction of the dermal layer of skin ( 154 , 192 – 194 ).…”

Section: Pathophysiological Importance Of the Selectinsmentioning

confidence: 99%

E-Selectin Ligands in the Human Mononuclear Phagocyte System: Implications for Infection, Inflammation, and Immunotherapy

2018

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The mononuclear phagocyte system comprises a network of circulating monocytes and dendritic cells (DCs), and “histiocytes” (tissue-resident macrophages and DCs) that are derived in part from blood-borne monocytes and DCs. The capacity of circulating monocytes and DCs to function as the body’s first-line defense against offending pathogens greatly depends on their ability to egress the bloodstream and infiltrate inflammatory sites. Extravasation involves a sequence of coordinated molecular events and is initiated by E-selectin-mediated deceleration of the circulating leukocytes onto microvascular endothelial cells of the target tissue. E-selectin is inducibly expressed by cytokines (tumor necrosis factor-α and IL-1β) on inflamed endothelium, and binds to sialofucosylated glycan determinants displayed on protein and lipid scaffolds of blood cells. Efficient extravasation of circulating monocytes and DCs to inflamed tissues is crucial in facilitating an effective immune response, but also fuels the immunopathology of several inflammatory disorders. Thus, insights into the structural and functional properties of the E-selectin ligands expressed by different monocyte and DC populations is key to understanding the biology of protective immunity and the pathobiology of several acute and chronic inflammatory diseases. This review will address the role of E-selectin in recruitment of human circulating monocytes and DCs to sites of tissue injury/inflammation, the structural biology of the E-selectin ligands expressed by these cells, and the molecular effectors that shape E-selectin ligand cell-specific display. In addition, therapeutic approaches targeting E-selectin receptor/ligand interactions, which can be used to boost host defense or, conversely, to dampen pathological inflammatory conditions, will also be discussed.

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E-selectin and vascular cell adhesion molecule-1 are critical for initial trafficking of helper-inducer/memory T cells in psoriatic plaques

Cited by 19 publications

References 0 publications

Retinoic acid inhibits the regulated expression of vascular cell adhesion molecule-1 by cultured dermal microvascular endothelial cells.

Retinoic acid inhibits the regulated expression of vascular cell adhesion molecule-1 by cultured dermal microvascular endothelial cells.

Inhibition of lymphocyte adhesion to cytokine‐activated synovial fibroblasts by glucocorticoids involves the attenuation of vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 gene expression

E-Selectin Ligands in the Human Mononuclear Phagocyte System: Implications for Infection, Inflammation, and Immunotherapy

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