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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK; Malden, USA : Blackwell Science Ltd/Inc.
    Contact dermatitis 50 (2004), S. 0 
    ISSN: 1600-0536
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Allergic contact dermatitis is a delayed type hypersensitivity reaction mediated by allergen specific T-lymphocytes. Allergen exposure leads to the activation of specific T-lymphocytes, which subsequently start to produce and release a vast array of cytokines and chemokines. However, the list of relevant genes taking part in the elicitation phase of contact dermatitis is not complete. In this study, we evaluate the use of the high-density microarray technology, which enable us to assess the global gene expression in allergen-stimulated peripheral blood mononuclear cells (PBMC). We included 3 chromium-allergic patients and 3 non-allergic controls in the study. Cultures of PBMC were established from each participant and stimulated with 100 ug/ul CrCl3 or media alone. The cell cultures were grown for 24 hours and the gene expression was analysed using an Affymetrix GeneChip(R) Array. Of the genes that exhibited differences of expression (p 〈 0.01) in allergen-activated PBMC from patients compared to controls, 54%(159/294) displayed increased activity and 46%(136/294) displayed decreased activity. Of the 159 up-regulated genes, 41 genes had a fold change above 1.50 and 30 genes among the 136 down-regulated genes had a fold change below -1.5. A significant number of the genes that showed differential expression in the cell cultures established from the allergic patients are known to be involved in immune responses and inflammation. The data indicates that the method of microarrays is a valuable tool for investigating the gene expression profile in our model system for allergic contact dermatitis.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary In this study we tested the capacity of ultraviolet B (UVB)-irradiated major histocompatibility complex (MHC) class II+ keratinocytes, monocytes and dendritic cells to activate T cells in the presences of Staphylococcus enterotoxin B. We demonstrated that UVB irradiation of MHC class II+ keratinocytes does not change their capacity to activate T cells in the presence of Staphylococcus enterotoxin B. In contrast. UVB irradiation of antigen T cells after UVB irradiation was not due to factors relased form UVB-irradiated cells. The interferon-γ induced uupregulation of HLA-DR and intercellular adhesion molecule-l on accessory cell function of interferon-γ pretreated monocytes. Differential requirements for and UVB regulation of costimulatory molecules may be involved. Since blocking of the B7/CD28 pathway affects the capacity of dendritic cells but not keratinocytes to activate T cells in the presence of Staphylococcus enterotoxin B. Thus. MHC class II+ keratinocytes in the presence of superantigens released from staphylococci may activate T cells and maintain inflammation despite UVB treatment.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    British journal of dermatology 147 (2002), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Background  Apoptosis has been proposed to act as an important mechanism for eliminating keratinocytes that have been irreversibly damaged by ultraviolet (UV) irradiation. One way to induce apoptosis in keratinocytes is through activation of the cell surface receptor Fas (CD95), either with the ligand (FasL) or directly with UV radiation. Objectives  To investigate the regulation of Fas and FasL expression in human skin and the formation of apoptotic cells after in vivo exposure to UVB or long-wave UVA radiation. Methods  Volunteers were irradiated with either 3 minimal erythema doses (MED) of UVB ( n  = 6) or 3 MED of long-wave UVA ( n  = 6) on buttock skin 12, 24 and 72 h before skin punch biopsies were taken. Expression of Fas and FasL was demonstrated by immunohistochemistry on cryostat sections. Apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated fluorescein-deoxyuridine triphosphate nick-end labelling reaction. Results  In five of six subjects, exposure to UVB radiation resulted in increased homogeneous expression of Fas on epidermal cells, with greatest expression at 24 and 72 h after irradiation. In all subjects, exposure to long-wave UVA resulted in increased homogeneous expression of Fas on epidermal cells, with greatest expression at 12 h after irradiation. In five of six subjects, exposure to UVB radiation resulted in temporarily decreased expression of FasL, but after 72 h the expression of FasL had returned to the preirradiation level. The expression of FasL on epidermal cells after exposure to long-wave UVA showed considerable variation. UVB irradiation was a stronger inducer of epidermal apoptosis than was UVA irradiation. The number of apoptotic epidermal cells did not correlate with expression of Fas or FasL. Conclusions  In human skin the expression of Fas on epidermal cells increases after in vivo exposure to UVB or long-wave UVA. Exposure to UVB causes a temporary decrease in the expression of FasL on epidermal cells.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Clinica Chimica Acta 168 (1987), S. 13-17 
    ISSN: 0009-8981
    Keywords: Diagnostic method ; Immunoradiometric assay ; Non-thyroidal illness ; Screening test ; Thyroid disease ; Thyroid stimulating hormone (TSH)
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 291 (1999), S. 247-252 
    ISSN: 1432-069X
    Keywords: Key words T cell activation ; Nickel ; Human ; Interferon-gamma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Contact hypersensitivity to nickel is the most common form of allergic contact dermatitis. To gain insight into the induction of this frequent disease, T cell reactivity towards nickel was investigated in “nonallergic” individuals defined as those with no skin manifestations and a negative patch test towards NiSO4. Surprisingly, we found that nickel induced proliferation of peripheral blood mononuclear cells (PBMC) from 16 of 18 adult individuals tested. This activation was specific, and no stimulation of PBMC was observed using control stimulants at equimolar concentrations. Furthermore, the NiSO4-induced activation required the presence of professional antigen-presenting cells. To describe the functional capacity of the nickel-inducible T cells, cytokine release was investigated in both nickel-allergic and nonallergic individuals. The T cells from both groups released interferon-γ but no interleukin-4 upon stimulation with nickel, suggesting that the functional capacities of these cell populations were similar in nickel-allergic and nonallergic individuals. Thus, at this level, no qualitative differences could be demonstrated between T cells obtained from nickel-allergic and nonallergic individuals.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 288 (1996), S. 255-257 
    ISSN: 1432-069X
    Keywords: Key words MHC class II+ keratinocytes ; IFNγ-treated ; skin ; Staphylococcal superantigen ; UVB irradiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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