UVA suppresses shedding of ICAM-1 from interferon-? (IFN-?)-pretreated transformed keratinocytes

Dummer, Reinhard; Jc, Meyer; Ballmer-Weber, BK; Muletta, S; Panizzon, R; Burg, Günter

doi:10.1007/bf00372015

Cited by 3 publications

(2 citation statements)

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“…Fur thermore UVA suppresses shedding of sICAM-1 from kéra tinocytes in vitro [26]. Therefore it could be speculated from our data that elevated serum sICAM-l found in atopic eczema patients before and after clinical remission might not be primarily of kératinocyte origin.…”

Section: Discussionmentioning

confidence: 79%

Elevated Serum Levels of Soluble Adhesion Molecules ICAM-1 and ELAM-1 in Patients with Severe Atopic Eczema and Influence of UVA1 Treatment

et al. 1995

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Background: ICAM-1 is known to be strongly expressed on keratinocytes in lesional atopic eczema correlating with the degree of inflammation. ELAM-1 was found to be expressed on dermal vascular endothelium in lesional atopic eczematous skin. Objective: The present study was performed to investigate whether elevated serum levels of soluble forms of these molecules are detectable in patients with severe atopic eczema and whether these parameters could be useful markers for disease activity. Methods: Serum levels of soluble ICAM-1 (sICAM-1) and ELAM-1 (sELAM-1) were measured by ELISA in 18 patients with severe atopic eczema before and after UVA1 therapy. Results: Before onset of treatment, serum sICAM-1 (565 + 99 ng/ml) and sELAM-1 (89.7 ± 29.9 ng/ml) levels were significantly (p < 0.001) elevated compared to 22 healthy control persons (296 ± 46 and 48.8 ± 22.7 ng/ml). After achievement of significant clinical improvement after 3 weeks of UVA1 therapy, there was neither a decrease in serum sICAM-1 nor in sELAM-1 levels. The posttherapeutic serum sICAM-1 and sELAM-1 values remained elevated (p < 0.001) above the normal range. Conclusion: Based on these data we suggest that (1) serum sICAM-1 and sELAM-1 are elevated in patients with severe atopic eczema, (2) sICAM-1 does not decrease together with reduction of ICAM-1-positive keratinocytes in atopic eczema following clinical improvement and might therefore be mainly of a different origin, i.e. leukocytes/endothelial cells, and that (3) sICAM-1 and sELAM-1 seem not to be suitable markers of actual disease activity in severe atopic eczema.

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Section: Discussionmentioning

confidence: 79%

Elevated Serum Levels of Soluble Adhesion Molecules ICAM-1 and ELAM-1 in Patients with Severe Atopic Eczema and Influence of UVA1 Treatment

et al. 1995

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“…These data point out that released adhesion molecules remain immunologically active proteins in a manner similar to sol uble cytokine receptors 115, 16]. Cytokines such as TNF-a and IFN-y induce ICAM-1 expression and release in mela noma cell lines, in the keratinocyte-derived HaCat cell line [17] and in most other cell lines. Other cytokines influence this process only marginally.…”

Section: Discussionmentioning

confidence: 94%

Various Cytokines Modulate ICAM-1 Shedding on Melanoma- and CTCL-Derived Cell Lines: Inverse Regulation of ICAM-1 Shedding in a Sézary Cell Line by Interferon-γ

et al. 1994

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Background: Since soluble intercellular adhesion molecules 1 (sICAM-1) retain their ability to bind to their ligand, they can interfere in cell-mediated immunosurveillance. Objective: We studied the impact of various cytokines on ICAM-1 release of several tumor cell lines. Methods: Two melanoma cell lines (M19, M26), 1 B lymphoblastoid cell line (Daudi), 1 erythroleukemia cell line (K562), 1 Sézary-cell-derived cell line (SeAx), 1 cell line derived from a mycosis fungoides lesion (MyLa) and normal peripheral blood mononuclear cells (PBMC) were grown in the presence of interferon γ (IFN-γ), IFN-α, interleukin-2 (IL-2), IL-6 and tumor necrosis factor α (TNF-α) in various concentrations. ICAM-1 release into the supernatant was measured after 24 and 48 h using an enzyme-linked immunosorbent assay (ELISA). Results: PBMC and the B lymphoblastoid cell line did not shed detectable amounts of sICAM-1. In all other cell lines, ICAM-1 shedding was found with and without cytokine stimulation. In all cell cell lines except the CTCL-derived one, ICAM-1 shedding was marginally affected by IFN-α, IL-2 and IL-6. TNF-α and IFN-γ enhanced the shedding in a time- and dose-dependent manner. In the SeAx line, IL-2 and IFN-γ inhibited ICAM-1 release. By contrast, TNF-α and IL-6 enhanced it. The CTCL-derived MyLa responded to IFN-α with a dose-dependent increase in ICAM-1 shedding. All other cytokines had marginal influence. Conclusion: Cytokine-modulated ICAM-1 shedding shows quantitative and qualitative differences in the investigated cell lines. This might have implications for the pathophysiology of cutaneous malignancies and their susceptibility to immunotherapies.

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Alterations in ICAM-1 and ELAM-1 expression in psoriatic lesions following various treatments

Danno

Kaji

Mochizuki

1996

Journal of Dermatological Science

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UVA suppresses shedding of ICAM-1 from interferon-? (IFN-?)-pretreated transformed keratinocytes

Cited by 3 publications

References 16 publications

Elevated Serum Levels of Soluble Adhesion Molecules ICAM-1 and ELAM-1 in Patients with Severe Atopic Eczema and Influence of UVA1 Treatment

Elevated Serum Levels of Soluble Adhesion Molecules ICAM-1 and ELAM-1 in Patients with Severe Atopic Eczema and Influence of UVA1 Treatment

Various Cytokines Modulate ICAM-1 Shedding on Melanoma- and CTCL-Derived Cell Lines: Inverse Regulation of ICAM-1 Shedding in a Sézary Cell Line by Interferon-γ

Alterations in ICAM-1 and ELAM-1 expression in psoriatic lesions following various treatments

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UVA suppresses shedding of ICAM-1 from interferon-? (IFN-?)-pretreated transformed keratinocytes

Cited by 3 publications

References 16 publications

Elevated Serum Levels of Soluble Adhesion Molecules ICAM-1 and ELAM-1 in Patients with Severe Atopic Eczema and Influence of UVA1 Treatment

Elevated Serum Levels of Soluble Adhesion Molecules ICAM-1 and ELAM-1 in Patients with Severe Atopic Eczema and Influence of UVA1 Treatment

Various Cytokines Modulate ICAM-1 Shedding on Melanoma- and CTCL-Derived Cell Lines: Inverse Regulation of ICAM-1 Shedding in a Sézary Cell Line by Interferon-&#947;

Alterations in ICAM-1 and ELAM-1 expression in psoriatic lesions following various treatments

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Various Cytokines Modulate ICAM-1 Shedding on Melanoma- and CTCL-Derived Cell Lines: Inverse Regulation of ICAM-1 Shedding in a Sézary Cell Line by Interferon-γ