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T J Stoof

Publications and source records attributed to T J Stoof.

At least 37 records · Page 2Linked to original sources
PubMed1997

The expression of interleukin-8 receptor in untreated and treated psoriasis.

The expression of IL-8 in psoriasis has been clearly shown with the use of immunocytochemical, RT-PCR and in situ hybridization methods. The presence of its ligand, the IL-8 receptor, has been demonstrated by the RT-PCR technique. We report here a study of the expression of both IL-8 type A and B receptors by immunohistochemical techniques, using one polyclonal and four monoclonal antibodies. By this technique, we found that the neutrophilic granulocytes express the IL-8 type A receptor, whereas the IL-8 type B receptor was present on the keratinocytes. The type B receptor on the keratinocytes was localized in the suprabasal layers of the epidermis. Following therapy, the expression of the IL-8 type B receptor on the keratinocytes was reduced. This could suggest that IL-8 in psoriasis is involved in the disturbed differentiation rather than in proliferation, probably via an autocrine loop.

Animals↗
PubMed1995

Pentoxifylline inhibits T-cell adherence to keratinocytes.

In many inflammatory dermatoses leukocyte function-associated antigen-1/intercellular adhesion molecule-1 mediated T-cell/keratinocyte adhesion is considered to play an important role. Pentoxifylline (PTX), a methylxanthine derivative widely used for the symptomatic treatment of various vascular disorders, was recently found to have anti-inflammatory effects. PTX can suppress tumor necrosis factor-alpha production and function, and inhibits leukocyte-endothelial cell adherence. The aim of the present study was to investigate whether PTX also interferes with T-cell/keratinocyte binding. Peripheral blood T cells were activated with phorbol myristate acetate and co-incubated with interferon-gamma- or tumor necrosis factor-alpha-stimulated keratinocytes (SVK 14 cells) in the presence or absence of PTX. Using an enzyme-linked immuno cell adhesion assay PTX was found to inhibit T-cell/keratinocyte adhesion in a dose-dependent manner. A similar inhibition was found when PTX was replaced by isobutylmethylxanthine, another methylxanthine derivative, or by a combination of two cyclic adenosine monophosphate analogues. No major effect on T-cell/keratinocyte adherence was observed when PTX was present during the pre-incubation of keratinocyte monolayers with tumor necrosis factor-alpha or interferon-gamma prior to the adhesion assay. In keratinocyte monolayers the interferon-gamma or tumor necrosis factor-alpha induced intercellular adhesion molecule-1 expression could not be inhibited by PTX. However, when PTX was added to short-term organ cultures of normal human skin biopsies, the lipopolysaccharide- and tumor necrosis factor-alpha-induced keratinocyte intercellular adhesion molecule-1 expression was blocked completely. The interferon-gamma-induced ICAM-1 expression was not blocked by PTX. The results presented herein suggest that impaired T-cell/keratinocyte binding may be one of the mechanisms by which PTX exerts a beneficial effect in certain inflammatory dermatoses.

1-Methyl-3-isobutylxanthine↗
PubMed1994

Human growth factor (huGRO), interleukin-8 (IL-8) and interferon-gamma-inducible protein (gamma-IP-10) gene expression in cultured normal human keratinocytes.

HuGRO, IL-8 and gamma-IP-10 belong to a recently described superfamily of genes encoding a group of cytokines with inflammatory, growth regulating and/or leukocyte chemotactic properties (chemokines). We studied huGRO, IL-8 and gamma-IP-10 gene expression in unstimulated and stimulated (TNF alpha, INF gamma, TNF alpha + IFN gamma, IL-1 beta, PMA and LPS) normal human keratinocytes by Northern blot analysis. The mRNA for none of the three chemokines was detectable in unstimulated keratinocytes, but considerably elevated levels of huGRO and IL-8 mRNA, but not of gamma-IP-10 mRNA, were found in the presence of cycloheximide, indicating that huGRO and IL-8 mRNA, but not gamma-IP-10 mRNA, are constitutively produced. gamma-IP-10 mRNA was exclusively induced by IFN gamma, with a strong and transient rise between 8 and 18 h, and superinduced by the combination of IFN gamma and TNF alpha, indicating marked synergism. Both huGRO and IL-8 mRNA were induced by TNF alpha and PMA (a strong and transient rise between 2 and 8 h), but not by IFN gamma or LPS. The combination of TNF alpha and IFN gamma did not show a synergistic effect. In addition, IL-1 beta transiently upregulated huGRO mRNA but failed to induce IL-8 mRNA. Using specific oligonucleotides for alpha, beta and gamma huGRO, TNF alpha was found to induce all three forms, alpha and beta to an equal extent and gamma to a lesser extent.(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed1994

Three cases of pemphigus vegetans: induction by enalapril--association with internal malignancy.

BACKGROUND: Pemphigus vegetans, a rare form of pemphigus vulgaris, consists of vegetating plaques localized to flexural areas. Two types, the Neumann and the Hallopeau type, are recognized with their own characteristics. METHODS: Three patients with pemphigus vegetans were examined, two with Hallopeau type and one with Neumann type. The microscopic and immunofluorescence findings were recorded. RESULTS: Two remarkable features were present. In one case pemphigus vegetans was possibly induced by the use of enalapril. Only in three previous cases has enalapril been described in relation to pemphigus. A second case was associated with a malignant lung tumor, a phenomenon which could not be traced in the literature. CONCLUSIONS: Two types of pemphigus vegetans must be distinguished. Induction of pemphigus (also vegetans) is an accepted side effect of captopril. The effect of enalapril on pemphigus is still in debate. To the best of our knowledge, this is the first time that a patient with pemphigus vegetans and a simultaneously occurring internal malignancy is described.

Aged↗
PubMed1994

Effect of calcitriol on growth, differentiation, chemokine mRNA expression of cultured keratinocytes and on keratinocyte-T cell binding.

Calcitriol has recently been shown to be effective against psoriasis. However, its mode of action is not exactly known. The present study focused on the influence of calcitriol on growth, differentiation, chemokine mRNA and ICAM-1 mRNA expression of keratinocytes (KC) and on the binding of T-cells to keratinocytes. In vitro studies showed that calcitriol has a strong anti-proliferative effect and induces terminal differentiation. gamma-IP-10 and ICAM-1 mRNA were induced by gamma-IFN, an induction not influenced by calcitriol. Moreover, the functional expression of ICAM-1 on the KC cell surface as measured by a cell adhesion assay, was not influenced either. IL-8 and huGRO mRNAs were constitutively produced in KC, as was demonstrated after incubation with cycloheximide. Up-regulation of both IL-8 and huGRO mRNA by IL-1 alpha was also not affected by calcitriol. It is concluded that calcitriol has a strong antiproliferative activity and does not interfere with KC responsiveness to gamma-IFN and IL-alpha induced chemokine expression or with the adhesion of T-cells to keratinocytes.

Calcitriol↗
PubMed1992

Keratinocyte activation following T-lymphocyte binding.

T lymphocytes infiltrate the epidermis and follicular epithelium adhering to keratinocytes within hours following induction of cutaneous inflammation. To determine if the physical binding interaction between a T cell and keratinocyte induces transmission of activation pathways, CD3+ T cells (HUT 78) were allowed to directly bind to non-cytokine-treated cultured keratinocytes. When these T cells bound to keratinocytes, the keratinocytes were activated as evidenced by detection of tumor necrosis factor-alpha, interleukin-6, and intercellular adhesion molecule-1 mRNA. This induction was relatively mRNA specific, as several other mRNA were not found to be altered. This activation process appeared to be one-sided, as no change in HUT cell mRNA levels was detectable. The keratinocyte activation process was confined to cultures that had direct physical binding by HUT cells, because co-culturing the HUT cells immediately above the keratinocyte monolayer (but not in direct contact), resulted in no such mRNA alterations. This direct adhesion-mediated activation of keratinocytes by T lymphocytes may be important in the genesis of cutaneous inflammation by amplifying the original stimulus, as well as contributing to the trafficking pattern of inflammatory cells as they leave the general circulation and enter the skin.

Cell Adhesion Molecules↗
PubMed1992

Sustained renal function loss in psoriasis patients after withdrawal of low-dose cyclosporin therapy.

Eight patients with psoriasis received low-dose cyclosporin (CyA) treatment for an average period of 12 months (range 4-16 months). There was great variability in minimal effective CyA dose. In 50% of the patients long-term treatment was limited by dose reductions necessitated by side-effects. A considerable impairment of renal function during CyA therapy was found. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured with 125I-iothalamate and 131I-hippuran, respectively. Both at the end of the active treatment period (GFR-CyA and ERPF-CyA), and 4 months after withdrawal of CyA (GFR-4mo and ERPF-4mo), there was sustained renal impairment: GFR-BL = 97 (64-117), GFR-CyA reduction 17.8% (2.2-31.9%) [P < 0.02], GFR-4mo reduction = 9.8% (5.5-21.5%) ml/min/1.73 m2 (P < 0.05 vs. BL); ERPF-BL = 401 (232-607), ERPF-CyA reduction = 10.1% (7.4-27.3%) [P < 0.05], ERPF-4mo reduction = 13.5% (3.0-32.9%) ml/min/1.73 m2 (P < 0.02). Further studies of the effects on renal function during, and after, long-term therapy of psoriasis with low-dose CyA are warranted.

Adult↗
PubMed1991

Detection of interferon-gamma mRNA in psoriatic epidermis by polymerase chain reaction.

Psoriatic skin lesions contain HLA-DR positive T lymphocytes, and other activation antigens, which suggest that the T cells may be producing lymphokines. Gamma interferon is produced by activated T cells, and its presence in psoriasis has been inferred by the lesional keratinocyte expression of 3 gamma interferon-inducible proteins i.e. HLA-DR, intercellular adhesion molecule-1, and gamma-IP-10. To determine whether gamma interferon is being produced directly in psoriatic lesions, punch biopsies of normal and diseased skin were separated into epidermal sheets and dermal fragments. Total cellular RNA was isolated from each epidermal and dermal compartment, and reverse transcribed followed by amplification of the resultant DNA by polymerase chain reaction. The amplification process involved the use of 5' and 3' primers for gamma interferon, and tumor necrosis factor-alpha, with beta-actin serving as a control. Gamma interferon mRNA, but not tumor necrosis factor alpha mRNA, was detectable in 4 of 5 psoriatic epidermal specimens. Neither mRNA was detectable in any normal skin dermal/epidermal specimens. Gamma interferon mRNA was also detectable in a single psoriatic dermal specimen. If reverse transcriptase was omitted, no polymerase chain reaction products were detected, indicating that the fragments detected were not derived from contaminating genomic DNA. These results indicate that gamma interferon mRNA can be extracted and successfully detected from human psoriatic lesional skin biopsies, using polymerase chain reaction technology. This molecular approach can easily be expanded to measure many other cytokines in both epidermal and dermal locations. The detection of gamma interferon in this clinical setting may be of particular pathophysiological significance because injection of gamma interferon has been reported to induce psoriatic lesions.

Actins↗
PubMed1990

Clear cell basal cell carcinoma.

We describe a case of clear cell basal cell carcinoma of the superficial type, presenting as a crusted eruption on the abdomen. Histological examination showed a solid proliferation of clear cells attached to the under-surface of an atrophied epidermis. In addition, distinct pagetoid infiltration was seen within the overlying epidermis. A focal connection between the clear cell portion and a deeper lying nodular basal cell carcinoma was demonstrated, elucidating the true nature of the lesion. Immunohistochemical studies and electronmicroscopy confirmed the epithelial derivation of the tumour. The clear cell appearance was due to multiple cytoplasmic electronlucent vacuoles which were not surrounded by membranes.

Abdomen↗
PubMed1989

Porokeratotic eccrine ostial and dermal duct nevus. Report of a case of adult onset.

We describe the case of a 38-year-old woman with adult-onset porokeratotic eccrine ostial and dermal duct nevus. The patient had a 9-year history of multiple keratotic papules and comedo-like pits on the medial border of the left foot. Light- and electron microscopic studies showed multiple cornoid lamella-like parakeratotic columns, which invariably were associated with hyperplastic eccrine ostia and distal sweat ducts. It is concluded that this entity, the first reported case of adult-onset porokeratotic eccrine ostial and dermal duct nevus, is a variant of the congenital form described previously by Abell and Read and by Aloi and Pippione.

Adult↗
PubMed1989

Does fish oil protect renal function in cyclosporin-treated psoriasis patients?

In order to study the influence of fish oil on CyA-induced renal dysfunction, 13 patients with psoriasis (CyA group) received cyclosporin A (CyA) alone, and seven patients (CyA/EPA + DHA group) received a combination of cyclosporin A and fish oil (6g eicosapentaenoic acid, C20:5 omega-3, and docosahexaenoic acid, C22:6 omega-3, daily) for 3 months. The glomerular filtration rate fell by 18.0 +/- 9.6% in the CyA group compared with 8.7 +/- 6.8% in the CyA/EPA + DHA group (mean +/- SD, P less than 0.05). The effective renal plasma flow fell by 10.6 +/- 8.9% in the CyA group and did not change in the CyA/EPA + DHA group (P less than 0.05). The calculated total renal vascular resistance increased by 19.8 +/- 14.5% in the CyA group and did not change in the CyA/EPA + DHA group (P less than 0.01). The results of this pilot study suggest that fish oil can reduce CyA-associated renal dysfunction in psoriasis patients.

Adult↗
PubMed1985

The induction of myeloid leukaemias by Rauscher murine leukaemia virus.

A number of cloned viral preparations isolated from Rauscher virus-producing JLS-V5 cells were compared in their competence to induce different types of leukaemias. All preparations were able to induce myeloid leukaemias, but the induction of lymphatic or erythroid leukaemias was also observed. Serial infection of newborn mice with either cell-free extracts or serum from animals suffering from a myeloid leukaemia did not result in the occurrence of relatively more myeloid leukaemias nor did the infection with virus harvested from ascites fluid of permanent myeloid cell lines. It appears that the mechanism by which myeloid leukaemias are induced is not virus-specific.

Animals↗
PubMed1982

Rauscher spleen focus-forming virus: biological properties and relationship to helper viruses.

A Rauscher virus (RV)-transformed erythroid cell line, RA-1, was shown to be a non-producer cell line. RA-1 cells express not only gp51-54 env-related glycoprotein, but also gp70, which is more closely related to gp51-54 coded by a recombinant env gene than to the MuLV-R gp70. RA-1 cells could be infected by Friend, Moloney and Gross viruses, but not by the homologous Rauscher murine leukaemia virus. Rescue of spleen focus-forming activity was obtained on infection of these cells with MuLV-F or MuLV-Mol, but not with MuLV-Gross. The RNA of the RV complex resembles closely that of Friend virus (FV). It contains a 32S, presumably defective, genome, which most likely is responsible for spleen focus formation, and a 35S helper virus genome. Oligonucleotide fingerprint data suggest that RV has evolved independently of FV. Erythroid early BFU-E cells of mice infected with RV of Friend helper virus-infected RA-1 cells were shown to require no addition of conditioned medium to form large erythroid colonies (BFU-E) in the presence of only small amounts of erythropoietin.

Animals↗
PubMed1981

The relationship between genomic RNAs of polycythaemic forms of spleen focus-forming Friend virus and its helper virus.

We have studied the relationship between Friend spleen focus-forming virus (SFFV) and its helper lymphoid leukaemia virus (LLV) by comparing RNase T1 fingerprints of genomic RNAs. Our data indicate that about 70% of the SFFV sequence is a perfect copy of parts of the helper genome. We conclude that our SFFV and LLV isolates have co-evolved very closely and that SFFV-specific sequences are not identical in different Friend virus isolates.

Base Sequence↗