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Substance P augments interferon-gamma (IFN-γ) but not tumor necrosis factor (TNF-α) mediated induction of keratinocyte ICAM-1 expression

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Page 1: Substance P augments interferon-gamma (IFN-γ) but not tumor necrosis factor (TNF-α) mediated induction of keratinocyte ICAM-1 expression

44 Oct. M/Concurrent Session 14 - Immunology: Inflammation and others

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198 DIFFERENTIAL EFFECTS OF ULTRAVIOLET B TREATMENT ON THE ADHESIVE PROPERTIES AND LIGAND EXPRESSION OF PSORIATIC DERMAL MICROVASCULAR ENDOTHELIAL CELLS. lian-Pine Cai, Keith Harris. L Richard T&or and Yee-Ho” Chm, Departments of Microbiology and Immunology, Dermatology and Curaneous Surgery, University of Miami, Miami, FL. U.S.A.

Psoriasis is characterized by intense CD4 T lymphocytic infiltrates. Our previous studies have shown that psoriatic dermal microvascular endothelial cells (DMEC), unlike normal DMEC, express endothelial ligands such as [CAM-I. ELAM-I and VCAM-1 and promote the specific adherence of memory T cell subset. Ultraviolet B (UVB) irradmtion is a msjor treaunent modality for psonasis, although the mechanism is unclear. In the present study, we compared the adhesive properrxs of DMEC in untreated and UVB-rreated psonauc plaques and correlated lymphocyte adhesion LO expressm” of ICAM-I, ELAM-I and VCAM-1. For this purpose, five patients with large plaque rype ofpsoriasis received UVB light treatment twice a day with a” initial dose of 20 ml/cm*, increaxd by 5 ml/cm2 dally. Peripheral blood and 4 mm punch biopsies were obtained before a”d during different periods of rreatment. Control patients were treated with emollient alone. The results showed that treatment of psoriatic plaques with UVB by day 6 decreased the adhesiveness of psoriatic DMEC for human T cells by ~-80% as compared to plaques mated with emollient alone. The decrease in binding was associared wnh reducnon in the expression of ICAM-I and ELAM-I on psoriatic DMEC. In contrast. the expression of VCAM-I on psoriatic DMEC was up- regulated following UVB treatmenr, implylng that lymphocyte binding is not promoted by lhls hgand. Interestingly, psoriarlc lesmns which were covered wirh occlusive dressings dunng UVB treatment also demonstrated similar decreases in the adhesion of lymphocytes and ICAM-I and ELAM-I expressm”. suggesting a systemic effect of UVB. Our finding supponed the hypothesis that UVB treatment may exert a therapeutic effect at the level of endothelial adheslvzness for lymphocytes.

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VCAM-1 IS INCREASINGLY EXPRESSED IN DERMAL NERVE FISRES DURING MVRINE EXPERIMENTAL CONTACT DERMATITIS Ute Hens&it. Kate” Mabnke. Johannes Roth and Clemens Sorg, Insttute of Experimental Dermatology, Unwersity of Miinster, Federal Republic of Germany “aswlar cell adhew,” molecule-1 (“CAM-1, IS know” to be ,“duced on cytokane- activated human endothelial cells and to medate adhesion Of mOnOn”Clear le”kOC”fes “la bindIng to the ,“tegr,” “LA-4. Recenr studies have show” fhat “CAM-I is a,$,, expressed on nonvascular cell types among them cultered human neural cells. To further elucidate the role of “CAM-1 in WY0 we l”“eSfigafed lmm”nOhi*tOChemiCally the expression Of “CAM-I during expernnenta, ,rr,tant ,ICD, and allerQ,C ,ACD, contact dermatitis of SALSic mice US#“Q mAb MIK-I .S against munne “CAM 3 Cryostat ear sections obtaIned at various time ooonts after lnductio” of ICD lcrof”” “ill or ACD lDNFSl were analvred for