摘要:

AbstractMammalian cell cytoplasm contains at least two proteins which bind retinoic acid (RA): CRABP I and CRABP II. Produced by separate cenes, they differ in their affinity for RA, their transcriplional regulation by R A, their tissue distribution, and possibly their function. They intervene, probably at different stages, in the “intracine” metabolic process which controls the amount of biologically active ligaml that is available for binding to the nuclear receptors of

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1993.tb00032.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractIn organotypic coculture of human epidermal keralinocyles (HEK) or follicular outer root sheath (ORS) cells with human dermal fibroblasts, a stratified epithelium develops which in many regards re‐sembles inleifollicular epidermis. The epithelium growing on type I collagen gels in the absence of a preformed basement membrane itself produces only low or moderate amounts of laminin and collagen type IV, so that a well‐structured basement membrane cannot be formed. This results in loose and insufficient anchoring of basal cells in the collagen gel, frequently leading to cleft formation at the junction. Because integrins are important receptors for cell‐cell and cell‐matrix adhesion of keratino‐cytes which under certain circumstances may also influence epidermal differentiation, we studied their expression under this culture condition which provides adhesional stress but leaves epidermal differentiation largely unaltered. The localization of integrins differed markedly from that in normal epidermis or normal outer root sheath since all integrin chains were polarized to the epithelium‐collagen I interface. Thus, not only the 7.6 and β4‐chains showed preferential expression at the basal attachment site of keratinocytes as in normal epidermis, but also the α2‐, α3‐, βM‐chains which in normal epidermis under “steady stale” conditions appeal‐primarily involved in cell‐cell interaction of keralinocytes and are preferen‐tially expressed at the lateral sides of their plasma membranes. Interest‐ingly, the altered expression of integrins in organotypic cultures is not accompanied by significant distu

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1993.tb00033.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractUsing ihe indirect immunohistochemical approach, the occurrence of γ‐melanocyte stimulating hormone (γ‐MSH)‐like immunoreactivily in human normal keratinocytes is described. The positive cells were observed in each layer of the epidermis (except stratum corneum) and often, at the level of the stratum spinosum, also around the orifices of cutaneous accessory organs, such as sweat glands and sebaceous glands/ hair follicles. Combining these data with our previous investigations, the results support the possibility that locally produced γ‐MSH could be involved in cutaneous immune response, pigmentation and epithelial pro‐liferation, as well as neu

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1993.tb00034.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractWe report on the immunophenotypical characterization of adult human skin transplanted onto severe combined immunodeficienl (SCID) mice. Thirty animals were followed for up to 12 months after receiving split‐thickness xenografts. of which 28 were tolerated for the whole test period. Antigen mapping revealed an almost complete preservation of human cellular and extracellular tissue components in long‐term trans‐plants including skin immune cells (Langerhans‐cells, macrophages. lymphocytes) and also parts of the engrafted endolhelium. Hence, xeno‐grafts on SCID mice offer a versatile experimental tool for the in vivo study of both human skin immune cell function and endothelial cell‐mediated interactions in an environment completely devoid of inter‐ferences by adoptive host im

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1993.tb00035.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractAmocrine and paracrine growth factors are important mediators in malignant transformation. Interferons (IFN) and retinoids (RX) are well‐known differentiative and immunomodulating agents with effects on subsets of different human tumors including malignant melanoma. In this study, we examined the modulating effects of three IFN and seven different RX on human melanoma cell lines regarding growth factor receptor expression. Growth factor receptor expression, including PDGF‐R, NGF‐R, EGF‐R, IR, IGF‐l‐R, TFR and c‐kil. was studied by immunhislochemistry and FACSsean analysis. Both groups of sub‐stances modulated the expression of some growth factor receptors. Upre‐gulation of PDGF‐R was seen after treatment with IFN as well as with RX. In contrast, EGF‐R was found to be downregulated in two EGF‐R‐positive cell lines by IFN and. on the other hand, induced by RX in two EGF‐R‐negalive cell lines. The expression of NGF‐R was modulated am‐biguously by these substances but demonstrated a cell line specificity in the different melanoma cell lines tested. Additionally, some of the tested growth factor receptors were not markedly changed regarding their ex‐pression by treatment with I

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1993.tb00036.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractNormal and chronic plaque psoriatic keralinocyte cultures were tested for theirin vitroresponse to 2–200 ng/nil TNF‐α and 0.1–10 ng/ml TGF‐β in a serum‐free culture system. All normal and lesional psoriatic epidermal cell cultures showed a dose‐ and lime‐dependent inhibition of growth in response to TNF‐α and TGF‐β. Inhibition in individual cultures was first seen at a concentration of 2 ng/ml for TNF‐α and 0.1 ng/ml for TGF‐β at day 2, but became significant at 20 ng/ml and 1 ng/ ml for TNF‐α and TGF‐β respectively at days 2‐6. This effect was statistically significant at days 3–4 for the group of normal (TNF‐α and TGF‐β, n = 10, p<0.01 and psoriatic cultures (TNF‐α. n = 9, p<0.0l; TGF‐β, n = 7, p<0.05). Epidermal cells from normal and psoriatic skin were inhibited to the same extent at the same optimal concentrations by each cytokine. Inhibition was abolished by the addition of specific antibody to each cytokine, whilst antibody to a different cytokine had no effect. Nuclear and/or nuclear membrane staining was observed with antibody to the p55 TNF receptor both in cultured keralinocyles and in the tipper epidermal layers of both normal and psoriatic skin. In contrast, plasma membrane and cytoplasmic expression of the p55 TNF receptor was observed on macrophages and lymphocytes infiltrating psoriatic der‐mis. This study has shown that the growth of normal and psoriatic keratinocytes was equally inhibited by TNF‐α and TGF‐βin vitro. The expression of TNF receptor by psoriatic keratinocytesin vivomay permit regulation of ep

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1993.tb00037.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

AbstractIt is generally accepted that tumor necrosis factor‐α (TNF‐α) is a multifunctional cytokine which is involved in the regulation of inflammation as well as immunity. In the present study, we investigated whether azelastine, a potent antiallergic agent, affects release of TNF‐α from peripheral blood mononuclear cells (PBMC) and U937 cell linein vitro. When human PBMC and U937 cells were stimulated by phytohemagglulinin (PHA) and 12‐0‐letradecanoyl‐phorbol‐13‐acetate (TPA). respectively, the cells released significant amounts of TNF‐α as determined by TNF‐α‐specific enzyme immunoassay. TNF‐α levels in the culture supernatant of PHA‐stimulated human PBMC and TPA‐activated U937 cells decreased in a dose‐dependent manner when these cells were cultured in the presence of azelastine. This inhibitory effect of azelastine was obtained at concentrations where the drug produced no toxicity. Moreover, azelastine also inhibited release of TNF‐α from U937 cells which were already activated by TPA. These results suggest that the inhibitory effect of azelastine on TNF‐α release plays an important role in its antiallergic action in addition to inhibition and/or antagonism of histamine and leukol

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1993.tb00038.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1993.tb00039.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY