Search PubMed⌕ Search

Biomedical subjects

J D Bos

Publications and source records attributed to J D Bos.

At least 109 records · Page 6Linked to original sources
PubMed1995

Repigmentation in vitiligo vulgaris by autologous minigrafting: results in nineteen patients.

BACKGROUND: Minigrafting is a successful therapy for localized vitiligo but has never been reported for vitiligo vulgaris. OBJECTIVE: Our purpose was to evaluate the efficacy of minigrafting in vitiligo vulgaris. METHODS: In 59 patients with stable vitiligo vulgaris, a minigraft test was done by implanting two minigrafts in the lesion to be grafted. Patients were selected for grafting when spread of pigment was observed within 3 months. The rate of repigmentation was evaluated by digital image analysis. RESULTS: Twenty-three patients (36 lesions), of 24 with a positive minigraft test, were grafted. The results of 19 patients were analyzed, showing 80% to 99% repigmentation in 14 lesions, 50% to 80% repigmentation in 10 lesions, and zero to 50% repigmentation in 12 lesions. Time of observation varied from 3 to 12 months after grafting. Best results were observed after 9 to 12 months. In all patients with a positive Koebner phenomenon depigmentation of the minigrafts developed. CONCLUSION: Autologous minigrafting is an effective therapy for stable vitiligo vulgaris in a selected group of patients.

Adolescent↗
PubMed1995

Cross-reactivity of human nickel-reactive T-lymphocyte clones with copper and palladium.

Twenty Ni-reactive T-lymphocyte clones were obtained from eight different donors and analyzed for their ability to cross-react with other metals. All Ni-reactive T-lymphocyte clones were CD4+CD8- and recognized Ni in association with either HLA-DR or -DQ molecules. Based on the periodic table of the elements, the metals Cr, Fe, Co, Cu, and Zn from the same horizontal row as Ni, and Pd and Pt from the same vertical row, were selected to study T-lymphocyte clone cross-reactivity. Distinct cross-reactivity patterns were found that could be divided into three major groups: Ni-reactive T-lymphocyte clones i) cross-reacting with Cu, ii) cross-reacting with Pd, or iii) without cross-reactivity. Major histocompatibility complex class II-restriction patterns of Cu- and Pd-induced proliferative responses did not differ from those for the Ni-induced responses. In vitro cross-reactivities with Cu and Pd may be favored by their bivalency and location next to Ni in the periodic table, and the similarity of these metals to Ni in binding to histidine residues of peptides in the pocket of major histocompatibility complex class II molecules. The present findings suggest that Cu and Pd hypersensitivities, which are occasionally observed in Ni-allergic patients, may be due to cross-reactivities at the T-cell clonal level rather than to concomitant sensitization.

Cells, Cultured↗
PubMed1995

Intercellular adhesion molecule-3 (CD50) on human epidermal Langerhans cells participates in T-cell activation.

Three different intercellular adhesion molecules (ICAMs) have been identified acting as ligand for counter-receptor leukocyte-function-associated antigen-1 (LFA-1) (CD11a/CD18). We have recently shown that ICAM-1 (CD54) is present on cultured human epidermal Langerhans cells but not on freshly isolated Langerhans cells, and that this molecule participates in the generation of an antigen-specific T-cell response. ICAM-2 (CD102) was not involved because this molecule is expressed by neither fresh nor cultured Langerhans cells. In this study, the presence of ICAM-3 (CD50) on Langerhans cells was examined. Flow cytofluorometric analysis demonstrated that ICAM-3 is strongly displayed by fresh Langerhans cells, and daily determinations showed that the level of this trypsin-resistant molecule remained nearly unchanged during in vitro culture for up to 4 d, indicating that Langerhans cells constitutively express this molecule. Analysis of RNA extracted from purified cultured Langerhans cells by means of reverse transcriptase-polymerase chain reaction demonstrated the presence of mRNA specific for ICAM-3. Antigen-specific T-cell responses triggered by Langerhans cells were dose-dependently inhibited by anti-ICAM-3 if the antibody was added within the first 16 h of T-cell stimulation. Simultaneous addition of anti-ICAM-1 and anti-ICAM-3 synergistically inhibited T-cell responses, although a total block was never achieved. Pretreatment of Langerhans cells with anti-ICAM-3 resulted in a reduced T-cell response, whereas pretreatment of T cells did not. These results suggest that ICAM-3 on Langerhans cells, like ICAM-1, is functionally involved in the initiation of antigen-specific activation of T cells, but the expression of these two ICAMs on Langerhans cells is differently regulated.

Antibodies, Monoclonal↗
PubMed1995

Demodicidosis or rosacea: what did we treat?

We report a 75-year-old man with a fulminant rosacea-like eruption, suggestive of demodicidosis. Multiple Demodex folliculorum mites were found in facial scales and pustules and, on histological examination, in the infundibulum of pilosebaceous follicles and in the dermis. Intradermal mites were surrounded either by polymorphonuclear granulocytes and histiocytes, or by a granulomatous infiltrate containing foreign-body giant cells, which had phagocytosed the parasites. Complete recovery, with disappearance of facial mites, was achieved by treatment with a combination of oral and topical metronidazole, although this drug is not known to be miticidal.

Aged↗
PubMed1995

Photoisomerization spectrum of urocanic acid in human skin and in vitro: effects of simulated solar and artificial ultraviolet radiation.

Ultraviolet (UV) irradiation of trans-urocanic acid (UCA), a major UV absorbing component of the epidermis, leads to the formation of cis-UCA, which mediates immunosuppressive effects. In this study, the net yield of cis-UCA was measured after the photoisomerization of urocanic acid by narrow UV wavebands (spectral range 295-405 nm), with the irradiation doses related to solar irradiance at sea level. The formation of cis-UCA in Caucasian skin (in vivo), as well as in aqueous solution (in vitro), was determined by HPLC analysis. The same irradiation conditions were met in both components of the study. The in vivo experiments showed high efficiency of cis-UCA formation in the spectral region of 305-341 nm, whereas high efficiency in vitro was found at 305 and 326 nm. At 350 and 363 nm, cis-UCA was formed in vivo, but not in vitro. At longer test wavelengths up to 405 nm, no significant formation of cis-UCA was detectable. The established partition between UVB and UVA at 320 nm is not relevant for the isomerization pattern of UCA. Additional studies revealed substantial cis-UCA formation in human skin by UVA phototherapy lamps. Furthermore, raised levels of 295 nm irradiation doses, a possible effect of stratospheric ozone depletion, were found to increase the cis-UCA yield. Our results demonstrate that the formation of cis-UCA in the skin with common exposures takes place over a broad spectrum range of UVB and UVA, up to at least 363 nm. These findings emphasize the potency of UVA to isomerize UCA, and they may contribute to further elucidation of the effects of phototherapy and sunbathing.

Chromatography, High Pressure Liquid↗
PubMed1995

A new psoralen-containing gel for topical PUVA therapy: development, and treatment results in patients with palmoplantar and plaque-type psoriasis, and hyperkeratotic eczema.

Topical photochemotherapy with psoralen and its derivatives 4,5',8-trimethylpsoralen (TMP) and 8-methoxypsoralen (8-MOP), with UVA irradiation, was evaluated with regard to minimum phototoxic dose, concentration, timing of UVA irradiation and systemic and local side-effects, in healthy volunteers. Psoralen (0.005%) in aqueous gel was found to be superior to TMP and 8-MOP in aqueous gel. No hyperpigmentation was seen after topical PUVA treatment with psoralen in aqueous gel. Patients with plaque-type psoriasis (n = 7), palmoplantar psoriasis (n = 7) and hyperkeratotic eczema (n = 2) were treated. Topical PUVA therapy was effective in most psoriasis patients, without the occurrence of local or systemic side-effects. Moreover, hyperkeratotic eczema patients who did not respond to conventional therapy showed partial remission. These results indicate that topical PUVA therapy with psoralen in aqueous gel is a useful therapeutic modality for treatment of psoriasis patients, and patients with recalcitrant dermatoses such as palmoplantar psoriasis and hyperkeratotic eczema.

Eczema↗
PubMed1995

Increased frequency and severity of angio-oedema related to long-term therapy with angiotensin-converting enzyme inhibitor in two patients.

Adverse reactions to drugs are well recognized as a cause of acute or chronic urticaria, and angio-oedema. Angiotensin-converting enzyme (ACE) inhibitors, used to treat hypertension and congestive heart failure, were introduced in Europe in the middle of the eighties, and the use of these drugs has increased progressively. Soon after the introduction of ACE inhibitors, acute bouts of angio-oedema were reported in association with the use of these drugs. We wish to draw attention to the possibility of adverse reactions to ACE inhibitors after long-term use and in patients with pre-existing angio-oedema.

Acute Disease↗
PubMed1995

Reduced antigen-presenting function of human Epstein-Barr virus (EBV)-B cells and monocytes after UVB radiation is accompanied by decreased expression of B7, intercellular adhesion molecule-1 (ICAM-1) and LFA-3.

In this study, the effect of ultraviolet-B (UVB) radiation on antigen-presenting function was studied, to investigate whether antigen-presenting cells (APC) are inhibited by UVB through a common mechanism. Two types of human APC were used: EBV-B cells and monocytes, and these were irradiated in vitro with single low doses of UVB (range 0-200 J/m2). Irradiation of EBV-B cells or monocytes resulted in similar dose-dependent reduction in APC function, when determined by the allogeneic mixed leucocyte reaction (MLR) or Candida albicans- or tetanus toxoid-specific T cell response. Our study shows that the reduced APC function was not likely to be caused by alterations in antigen processing or cytokine production. However, UVB-irradiated APC displayed marked changes in adhesion molecule expression. Irradiated EBV-B cells showed reduced expression of ICAM-1 (30%), LFA-3 (25%) and B7-1 (35%), while expression of HLA-DR, CD19 and LFA-1 was not affected. UVB irradiation of monocytes did result in reduction in the expression of HLA-DR (30%), LFA-3 (40%), ICAM-1 (65%) AND B7-1 and B7-3 (90%), but had no effect on CD14, LFA-1 and ICAM-3 expression. Addition of non-irradiated cells (but not the supernatant of these cells) or CD28 antibodies partly restored T cell activation, indicating that UVB-induced reduction in APC function is at least partly mediated via impairment of co-stimulatory molecule expression.

Antigen Presentation↗
PubMed1995

In situ behavior of human Langerhans cells in skin organ culture.

BACKGROUND: Epidermal Langerhans cells (ELC) play a critical role in the initiation of cutaneous immune responses. ELC are characterized by the expression of major histocompatibility complex (MHC) class II Ag and a number of adhesion/costimulatory molecules. Evidence suggests that cytokines induced within the epidermis regulate the functions of ELC, including their phenotypic expression. In the human system, no information is available regarding the behavior of the ELC in situ: their changes in morphology, expression of functional molecules or migration within the microenvironment. In the present study, using an ex vivo human skin organ culture model, we addressed the above questions and also examined the phenotypic modulation of ELC in situ by cytokines. EXPERIMENTAL DESIGN: Skin explants were cultured either in a Trowell-type method or free in the medium. Skin explants were cultured with and without cytokines and were processed for light and electron microscopy and for immunohistochemical definition of ELC phenotypes. RESULTS: In the Trowell-type skin organ culture, morphologic integrity of ELC, CD1a molecule, and Birbeck granules could be preserved intact up to 3 to 4 days in culture. During the first 3 days of culture, the intensity of MHC-II (HLA-DR, DP, and DQ) and CD1a expression on ELC increased sharply, and the dendritic appearance of ELC became more prominent at Day 3. Adhesion molecules, ICAM-1, LFA-3, HECA-452, sLx, and B7/BB1 were also spontaneously acquired in varying amounts by CD1a+ ELC after 3 days in culture. Significant increase of CD1a and ICAM-1 expression on ELC was observed within 12 hours, when skin explants were cultured free in the medium with GM-CSF and TNF-alpha, respectively. Further, we demonstrated spontaneous migration of ELC within the epidermis and then to the dermis during the Trowell-type skin culture. We also showed the migration of ELC out of the human skin when skin explants were cultured directly in the medium. CONCLUSIONS: Human ELC showed significant phenotypic changes within the epidermis and acquired migratory capacity during the skin organ culture. ELC in skin organ culture appear to undergo a phenotypic maturation within the epidermis. ELC in situ rapidly respond to GM-CSF and TNF-alpha by increasing the expression of CD1a and ICAM-1 molecules, respectively. These results suggest the modulation of phenotypic characteristics of ELC and their migration in response to the changes of epidermal microenvironment and cytokines and implicate the potential use of skin organ culture model to elucidate the role of human ELC in the immunopathology of skin diseases.

Antigens, CD1↗
PubMed1994

Function of adhesion molecules lymphocyte function-associated antigen-3 and intercellular adhesion molecule-1 on human epidermal Langerhans cells in antigen-specific T cell activation.

In addition to the interaction between the TCR and the MHC/Ag complex on the APC, optimal T cell activation also requires interaction between adhesion molecules on the APC and their ligands on T cells. We determined the presence of adhesion molecules on human epidermal Langerhans cells (LC) and their role in Ag-specific T cell activation. Freshly isolated LC did not display ICAM-1 (CD54), ICAM-2, LFA-1 (CD11a), and LFA-3 (CD58), as detected by double-color FACS analysis, using HLA-DR expression for LC identification. Upon culture, LC clearly expressed ICAM-1 and LFA-3, both already detectable after 1 day, reaching a plateau at day 2. ICAM-2 and LFA-1 were undetectable on cultured LC and attempts to induce this expression by different culture conditions remained unsuccessful. mAb against ICAM-1, LFA-1, LFA-3, and CD2, continuously present during culture, inhibited the T cell proliferative response to Candida albicans presented by cultured LC. Pretreatment of LC and/or T cells with mAb indicated that anti-ICAM-1 and anti-LFA-3 inhibited at the LC level, whereas anti-LFA-1 and anti-CD2 inhibited at the T cell level. The mAb-induced inhibition was dose-dependent, but a total blockade of the response was never achieved. Time-course observations revealed that ICAM-1 and LFA-3 on LC only functioned during the initiation phase of T cell activation. Our study demonstrates that both ICAM-1 and LFA-3 on LC considerably contribute to the generation of a T cell response. The high expression of these accessory molecules enable LC, at least in part, to perform their powerful Ag-presenting function.

Antigen-Presenting Cells↗
PubMed1994

Glycosylphosphatidylinositol (GPI)-anchored membrane proteins are constitutively down-regulated in psoriatic skin.

Hyperproliferation of keratinocytes (KCs) in psoriasis has been found to be associated with excessive activation of a phospholipase C (PLC)/protein kinase C (PKC) signal transduction system. The molecular species of PLCs which are activated in psoriasis have not been thoroughly investigated. It was envisaged that if glycosylphosphatidylinositol (GPI)-specific PLC was activated in the membrane of psoriatic epidermal cells, it would render these cells devoid of those proteins which are anchored to the cell membrane through their GPI moiety. In order to test this possibility, four GPI proteins (CD16, CD55, CD58, and CD59) were determined immunohistochemically in normal and psoriatic skin. In normal skin, CD55 and CD59 were strongly expressed on epithelium and vascular structures, whereas CD16 and CD58 were strongly expressed only on epithelium. The expression of all four GPI proteins was decreased in non-lesional psoriatic skin and virtually abolished in lesional psoriatic skin. A control transmembrane protein, CD46, was strongly expressed in normal and non-lesional psoriatic skin, and its expression was not significantly decreased in psoriatic lesions. The absence or reduction of GPI proteins was not seen in the lesions of several other inflammatory and proliferative diseases studied.

Adolescent↗
PubMed1994

The skin immune system: lupus erythematosus as a paradigm.

Lupus erythematosus (LE) was first described as a clinical dermatological entity in 1851. The possibility of serious systemic manifestations became recognized by 1872 as the result of the work of M. Kaposi. Since then, it took a long time before LE was recognized to be an immunological disease. Recognition of antinuclear antibodies and their deposition at the basal membrane region in skin resulted in two concepts of LE pathogenesis. In one, antibody complexing and complement activation with generation of the membrane attack complex (C5-C9) is thought to be the origin of the chronic inflammatory reaction. In the other, antibody deposition enables antibody dependent cellular cytotoxicity, leading to hydropic degeneration of the basal epidermal layer and subsequent chronic inflammation. Norris postulated in 1993, that the epidermis acts as a pro-inflammatory organ, in which an UVB-induced increase in cytokine production is followed by increased expression of adhesion molecules on keratinocytes as well as dermal endothelial cells. Translocation of certain antigens (i.e. Ro & La) to which circulating auto-antibodies exist in LE, enables recognition by adhesion molecule directed skin-invading T cells with subsequent cytotoxic effector activity. A persistent chronic inflammatory reaction then ensues. A similar development in knowledge may be seen in the history of immunodermatology. Originally, lupus erythematosus could not be recognized as an immune disease, since concepts of immunology were virtually non-existent when LE was first described. Immunology, In the first half of this century, was mainly antibody-oriented and thus came the concept of (S)LE as an antibody-mediated disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Allergy and Immunology↗
PubMed1994

Reappraisal of in situ immunophenotypic analysis of psoriasis skin: interaction of activated HLA-DR+ immunocompetent cells and endothelial cells is a major feature of psoriatic lesions.

Psoriasis is an inflammatory skin disease of unknown aetiology. Many observations indicate that T cells play an important role in the pathogenesis of the disease. Upregulation of MHC class-II molecules on immunocompetent cells, endothelial cells and keratinocytes on lesional psoriatic skin has been regarded as a hallmark of the disease. However, there is some controversy in the literature regarding the cell types expressing class-II molecules and there is limited information about the presence of immune cells other than T cells and antigen presenting cells in the cellular infiltrates of psoriatic skin. We therefore reinvestigated the subject using immunocytochemical single and multiple staining techniques. In agreement with earlier reports, our studies showed that the cellular infiltrates in lesional skin consist largely of HLA-DR+/IL-2R+ T cells, HLA-DR+/CD1a+ Langerhans cells, and HLA-DR+/CD68+ macrophages. We found increased HLA-DR expression mostly on immuno-competent cells and endothelial cells, but no prominent HLA-DR expression on keratinocytes in lesional psoriatic skin. Upregulation of HLA-DR on endothelial cells and in mononuclear infiltrates was also evident in the non-lesional skin of psoriatic patients as compared with normal controls. B cells and natural killer cells were also found in the cellular infiltrates in lesional psoriatic skin. In spite of the presence of a large amount of activated T cells in the epidermis, we found that HLA-DR expression on keratinocytes was not a major feature of psoriatic skin.

Adult↗
PubMed1994

Increased expression of adhesion receptors in both lesional and non-lesional psoriatic skin.

Adhesion receptors and their ligands play a vital role in the immune system. We studied the expression of different adhesion receptors, using single- and double-staining immunohistochemical techniques, in both lesional and non-lesional skin specimens from seven psoriasis patients and in skin biopsy specimens from eight normal healthy controls. Our results showed an overall increased expression of several adhesion receptors in both lesional and non-lesional psoriatic skin. We consistently found an increased expression in particular of ICAM-1 and E-selectin on endothelial cells, and ICAM-1 on T cells and Langerhans cells. In contrast, a weak expression of VCAM-1 was found on endothelial cells and mononuclear cells in lesional psoriatic skin specimens alone. Interestingly, LFA-1 was also expressed on Langerhans cells, with a greater frequency in skin from lesional than from non-lesional sites, but was never expressed in skin from normal healthy individuals. Furthermore, significantly increased numbers of Langerhans cells and T cells with a positive reactivity for MAb HECA-452 were found in both lesional and non-lesional psoriatic skin. We hypothesize that the enhanced expression of adhesion receptors on migrating immunocompetent cells and endothelial cells of psoriatic skin in general facilitates the increased influx of activated T lymphocytes and other immunocomponent cells into the skin, and thus underscores the generalized character of the disease.

Adult↗
PubMed1994

Contact allergy to corticosteroids: the results of a two-centre study.

We report a comparative study of the patch-test results obtained with a corticosteroid series, added to the standard series, in two centres, one in Belgium and the other in the Netherlands. The frequencies of positive reactions to the corticosteroids differed considerably between the two centres, and we suggest several reasons for this.

Adrenal Cortex Hormones↗
PubMed1994

Morphoea lesions are associated with aberrant expression of membrane cofactor protein and decay accelerating factor in vascular endothelium.

One of the main features of systemic and localized forms of scleroderma is vascular damage, the mechanism of which is not yet understood. Recently, we have shown undetectable or decreased expression of complement regulatory molecules, membrane cofactor protein (MCP) and decay-accelerating factor (DAF), in cutaneous endothelium of patients with systemic sclerosis (SSc). In some patients, CD59 expression in endothelium was also altered. As these molecules protect endothelial cells from damage by autologous complement, their decreased expression could be part of the mechanism of vascular damage in SSc. In the present study, we investigated the expression of MCP, DAF and CD59 in the endothelium of lesional and non-lesional skin of patients with localized morphoea. Normal skin and lesional skin from patients with systemic lupus erythematosus, and three inflammatory diseases, were included as relevant controls. The results showed that the extent of expression of the three molecules in non-lesional skin of patients with morphoea, on all the skin cells and structures, was identical to that of normal skin. In lesional skin, however, the expression of MCP and DAF in endothelium was either undetectable or only present to a very slight degree. CD59 expression in endothelium in lesional skin was normal. No such aberrant expression was observed in the lesions of any of the control diseases. These results indicate a decreased ability of endothelial cells in lesional areas to protect themselves from autologous complement, and this could contribute to vascular damage in morphoea lesions.

Antigens, CD↗