摘要:

AbstractIt has recently become clear that cyclin‐dependent kinase (cdk) complex regulates the cell cycle by phosphorylating Rb protein, a tumor suppressor protein. It is likely that this complex is a target of various growth factors and anti‐growth factors (UV TGF‐β etc.) in keratinocyte (KC). It has also been suggested that abnormalities in the cell cycle regulating mechanism such as increased activity of cyclin‐cdk due to mutation of p53, a tumor suppressor gene, and overexpression of cyclin D may be concerned with carcinogenesis of KC. Thus, recent studies indicate that the cyclin‐cdk complex is a common target of proliferation and carcinogen

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1995.tb00215.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractWe examined epidermal impairment in photodamaged Caucasian skin by light and electron microscopy and observed two types of degeneration of the basal and suprabasal keratinocytes. The first was an electron‐lucent degeneration predominantly seen in the periphery of the cells. The marked lucent degeneration occurred in 14% of the basal and suprabasal keratinocytes, predominantly in cells immediately adjacent to melanocytes. In skin specimens with a large number of such damaged keratinocytes, bleb‐like keratinocytic protrusions or electron‐lucent intercellular structures were also seen. Many vacuolar structures were observed just under the dermoepidermal junction, occupying 9% of the junction length. These structures were produced by hernialion of the degenerative portion of the basal and suprabasal keratinocytes, and appeared to be phagocytized by dermal macrophages. The vacuolar alterations in the basal layer and dermoepidermal junction previously reported at the light microscopic level probably represent these intercellular lucent structures, bleb‐like protrusions and vacuole‐like structures at the electron microscopic level. The second type, dark‐staining keratinocytes, probably representing an extensive degenerative process, constituted 4% of the basal and suprabasal keratinocytes. After 12 months of topical trelinoin treatment, dramatic improvement of both degenerative processes of the keratinocyte

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1995.tb00216.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractThe depigmenting C57BL/6J‐mivit/mivit) (mivit/mivit) mouse, a congenic mutant of the C57BL/6 strain, exhibits an isolated, single immune deficiency. It is unable to mount a normal immune/inflammatory response upon epicutaneous application of DNFB or TNCB, although it does respond normally to oxazalone. The present investigtions have been carried out to further study this deficiency.In vivo, C57BL/6 mice could be sensitized by the epicutaneous application of the hapten TNCB, the subcutaneous injection of haplen(TNBS)‐conjugated C57BL/6, and hapten conjugated mivit/mivitepidermal cells. In the mivit/mivitmice, however, only subcutaneous injection of haptcnizcd C57BL/6 epidermal cells caused an immune response. The response of these mivit/mivitmice could be documented only by adoptive transfer of splenic lymphocytes into naive C57BL/6 animals which then reacted to challenge doses of TNCB. These observations suggest that mivit/mivitepidermal cells can process and present and mivit/mivitT lymphocytes can react to the antigen. We postulated the presence of a deficient in vivo interaction between epidermal cells and T lymphocytes in the mivit/mivitmice. ICAM‐I is an important adhesion signal regulating epidermal cell/T‐lymphocyte interaction. Us expression in mivit/mivitmice was studied using YN1/1 antibody against MALA‐2, the murine counterpart of human ICAM‐1. In contrast to C57BL/6 animals, the mivit/mivitepidermis essentially did not stain with the antibody after hapten challenge.In vitroafter stimulation with TPA or IFN‐γ, the mivit/mivitepidermal cells expressed significantly lesser amounts of ICAM‐1 than the C57BL/6 epidermal cells. Lower expression of ICAM‐1 by mivitmivit/mivitsol;mivitepidermal cells has also been demonstrated both by direct staining and by flow cytomelry. The binding of lymphocytes to mivit/mivitepidermal monolayers, which were stimulated to express ICAM‐1 by IFN‐y, was decreased compared to that of C57BL/6 epidermal cells. We conclude that the muted contact sensiliza‐tion response detected in vivo in the mivit/mivitmice at least partly results from lower expression of ICAM‐1 and thus defective epidermal ccl

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1995.tb00217.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractUnregulated expression of epidermal growth factor receptor (EGF‐R) is a common event in neoplastic transformation and has been shown to be associated with melanocytic tumor progression. Modulation of such a receptor by pharmacological agents could therefore be of clinical interest. We have studied EGF‐R expression, its response to epidermal growth factor (EOF) and modulation effects by interferon gamma (IFNγ) on human melanoma cells. Addition of EOF, anti‐EGF and anti‐EGF‐R antibodies had no effect on proliferation of six melanoma cell lines tested. We report in this communication that EGF‐R expression on human melanoma cells can be modulated by IFNγ. In the melanoma cell lines treated with IFNγ. proliferative behavior was not affected; however, we demonstrate a downregulation of EGF‐R expression on the protein level, by immunohistochemistry and flow cytometric analysis, and an accumulation of EGF‐R mRNA by Northern blot analysis. The results suggest that IFNγ downregulates EGF‐R expression at a posttranscriptional level on human melanoma cells. This EGF/EGF‐R interaction and its modulation by IFNγ on human melanoma cells needs to be further clarified regarding itsin vivosignificance for the treatment and prognos

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1995.tb00218.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractTo determine the therapeutic mechanism of PUVA in psoriasis vulgaris, the effects of PUVA on activated T lymphocytes were investigated in vitro. Peripheral blood mononuclear cells (PBMC) obtained from healthy volunteers were activated with Con A stimulation (Con A blasts). Both untreated PBMC and Con A blasts were irradiated with UVA light in the presence of 8‐methoxypsoralen (8‐MOP). The expressions of CD4, CDS, VLA‐4 and LFA‐1 of PBMC and Con A blasts were stained with each monoclonal antibody and the intensity of fluorescence was analyzed by FACScan. PUVA‐treated PBMC showed decreased response to both Con A and PHA stimulation. PUVA treatment also suppressed the IL‐2 production of Con A blasts and IL‐2 response of PBMC with increasing UVA fluence. The expressions of LFA‐I, VLA‐4, CD4, CDS and CD25 (IL‐2R) molecules were decreased in PUVA‐treated Con A blasts. Con A blasts were more sensitive than untreated PBMC to PUVA treatment. These results suggest that the therapeutic effects of PUVA on psoriasis vulgaris can be induced by suppression of the expression of cell surface molecules of ac

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1995.tb00219.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractWide variations in susceptibility to skin tumor development by chronic ultraviolet light (UV) exposure and antigenicity of induced tumors which is estimated by tumor rejection in syngeneic recipients have been recognized among various murine strains. To examine the effect of parent genetic background on latency and antigenicity of UV‐induced tumors originating in F1hybrids, we induced skin tumors in three mouse strains: BALB/c, C57BL/6, (B6), and C3H/HeMs (C3H/He), and their F1, hybrids: (BALB/c×C3H/He)F1, (CC3F1), (BALB/c×B6)F1, (CB6F1) and (C3H/He×B6)F1, (C3B6F1) by exposing mice to UV radiation (0.44 mW/ cm2for 1 h) three times a week, and analyzed whether the UV‐induccd tumors originating in F1hybrids possess the similar property in latency or antigenicity as seen in the UV‐induced tumors derived from the parent strains. The latency of tumor induction by chronic UV exposure in C3H/He, BALB/c and their F1, hybrid CC3F1, was relatively short whereas that of B6 was relatively long, and that of F1, hybrids with B6 (CB6F, and C3B6F1) was intermediate. On the other hand, the low antigenicity as progressive growth behavior of UV‐induced tumors in syngeneic recipients was observed not only in tumors derived from C3H/He but also in those from F, hybrids with C3H/He (C3B6F1, and CC3F1) whereas most tumors derived from B6, BALB/c and their F1hybrid CC3F1were highly antigenic as to be rejected in syngeneic recipients. These findings suggest that the parent genetic quality regulating the susceptibility to tumor induction by chronic UV exposure is co‐dominantly inherited into F1hybrids. On the other hand, that providing the progressive growth behavior of induced tumors appears to be a dom

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1995.tb00220.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractThere is a need in many studies on the epidermal permeability barrier for practical and reliable separation of all major fractions of human stratum corneum lipids. Various methods have been described including thin layer chromatography, high performance thin layer chromatography and iatroscan. However, none of these methods seems to be applicable for an inexpensive, rapid and reliable analysis of a large number of samples. Here, such a method for the separation and quantification of all major stratum corneum lipid fractions is presented. This method employs the one‐dimensional separation of stratum corneum lipids using thin layer chromatography. The systems used herein are based upon various modifications of the solvents, solvent ratio and developing distance of each system. For quantification of chromatographed and charred lipids a Desaga densitometer is used. The system described here had been successfully applied to 550 samples of human stratum corneum lipid

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1995.tb00221.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractIt has been proposed that interleukin‐6 may play a role in the pathogenesis of autoimmune diseases like lupus erythematosus. We have therefore investigated the immunoreactivity of IL‐6 in 32 skin biopsies of 23 patients suffering from chronic discoid lupus erythematosus (n=16), subacute cutaneous lupus erythematosus (n=5) and systemic lupus erythematosus (n = 5) as well as in uninvolved skin (n = 6) and in normal skin from healthy volunteers (n = 3). Increased immunohistochemical staining was detectable in 14 of 26 biopsies from lesional skin. The remaining biopsies from lesional, non‐lesional and normal skin displayed only minimal or no reactivity, but 8 out of 12 lupus erythematosus patients had been pretreated with local or systemic antiinflammatory drugs. Irrespective of the LE subtype, immunolabelling was generally most intense in the basal layer of the epidermis, with additional intense suprabasal staining in sections from 2 of 5 SLE patients. Preferential production of IL‐6 in the lower parts of the epidermis was confirmed by RNAin situhybridization. No correlation was found between the deposition of immuno‐globulins and complement at the dermo‐epidermal junction and IL‐6 expression in keratinocytcs. These data suggest that IL‐6 may be involved in LE although its exact role in the pathogenesis of the disease needs to be fur

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1995.tb00222.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractPachydermoperiostosis (POP) is a hereditary disease with hy‐perostosis, clubbing of fingers, coarse skin and thickening of bones. Previous studies have disclosed some abnormality in the connective tissue in these patients. The purpose of the present study was to investigate connective tissue pathology in one family with PDP using libroblasl cultures. Fibroblastic cells were established from both the affected and healthy looking skin of 2 patients with PDP, and the expression of types I and III collagen, 92 kDa and 72 kDa gelatinases, metalloproteinase inhibitor (TIMP‐1), human retinoic acid receptor and transforming growth factor β (TGFβ) was analyzed. The modulation of glycoprolein synthesis, and of plasminogen activators and their inhibitors by TGFβin vitrowere also studied. The results indicated that collagen genes and gelatinases were similarly expressed in PDP and control cells, as well as the human retinoic acid receptor. TGF‐β stimulated, both in PDP cells and normal cells, the synthesis of fibroneclin, procollagen and plasminogen activator inhibitor‐1 (PAI‐1), but qualitative differences could not be found. Proteolytically processed forms of PAI‐1 were detected in

ISSN:0906-6705    

DOI:10.1111/j.1600-0625.1995.tb00223.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY