Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion receptors on endothelial cells are considered to be important for cellular influx in tissue. In this regard, skin constitutes a specialised environment for migration of leukocytes during inflammation. Using immuno-enzymatic staining techniques, we compared the in situ expression of ICAM-1, E-selectin, and VCAM-1 on endothelial cells and inflammatory infiltrates in both lesional and non-lesional biopsied skin from two immuno-inflammatory diseases, viz. psoriasis and contact dermatitis. The results were compared with those in skin specimens obtained from normal healthy individuals free from any history of skin disease. Our results show that ICAM-1 and ELAM-1 are upregulated in psoriatic non-lesional and lesional skin. On the other hand, in non-lesional biopsy from contact dermatitis patients, all three AR molecules are sparsely present, similar to the situation in normal skin although they are overtly expressed in the lesional sites. Moreover, VCAM-1 was found to be significantly increased on endothelial cells in the lesional sites of contact dermatitis as compared with biopsied psoriatic specimens. Interestingly VCAM-1 was also found to be present on some T-cells and Langerhans cells in contact dermatitis alone. The present data suggest that in different inflammatory dermatitis, varying adhesion receptor-ligand interactions involving endothelial cells and leukocytes are involved, which may be due to the differing cytokine profiles of perivascularly located T-cells.
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PMID:Differential expression of ICAM-1, E-selectin and VCAM-1 by endothelial cells in psoriasis and contact dermatitis. 752 Nov 4

Adhesion molecules are essential for the recruitment of T cells into the skin during the development of graft-vs-host skin disease (GVHSD). However, the mechanisms responsible for the regulation of expression of cutaneous adhesion molecules in this setting are still poorly understood. In this study we blocked lymphotoxin (LT) signaling in a murine model of minor histocompatibility Ag system mismatch GVHSD by using an LTbeta receptor-Ig fusion protein (LTbetaR-Ig). The recipient mice treated with control human Ig developed clinically apparent, severe skin lesions. However, none of the mice treated with LTbetaR-Ig developed clinical skin disease. The expression of ICAM-1 in cutaneous tissue was also much lower in mice treated with LTbetaR-Ig than in mice treated with human Ig. Thus, the inhibition of LT signaling via LTbetaR-Ig treatment appears to be capable of markedly ameliorating the development of GVHSD, possibly by inhibiting the expression of adhesion molecules.
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PMID:Blockade of lymphotoxin signaling inhibits the clinical expression of murine graft-versus-host skin disease. 1473 44