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J D Bos

Publications and source records attributed to J D Bos.

At least 127 records · Page 7Linked to original sources
PubMed1994

Linear connective tissue naevus of the proteoglycan type ('naevus mucinosus').

We report a case of naevus mucinosus, a recently described condition. Clinically, the lesions presented as unilateral, multiple, firm, 3-5-mm-diameter, coalescent papules in a linear arrangement on the back of a 23-year-old man. Histologically, large amounts of acid mucopolysaccharides (proteoglycans) were demonstrated in the superficial dermis. As far as we are aware, this is the first report of the onset of naevus mucinosus in an adult. Naevus mucinosus appears to be a distinct type of connective tissue naevus which is characterized by an increase in proteoglycans.

Adult↗
PubMed1994

Aberrant expression of membrane cofactor protein and decay-accelerating factor in the endothelium of patients with systemic sclerosis. A possible mechanism of vascular damage.

BACKGROUND: One of the main features of systemic sclerosis (SSc) is vascular damage, the mechanism of which is not understood. The aim of this study was to investigate if complement (C) regulatory molecules, membrane cofactor protein (MCP), decay-accelerating factor (DAF), and CD59, which normally protect endothelial cells from damage by autologous C, are absent or down-regulated in vascular endothelium of patients with SSc. A deficiency or persistent down-regulation of the above molecules is likely to render vascular endothelium of these patients susceptible to damage by physiologically or pathologically activated C. From this point of view, expression of MCP, DAF, and CD59 was tested on endothelium of skin of normal subjects and patients with diffuse and limited forms of SSc. EXPERIMENTAL DESIGN: Punch biopsies of normal skin (N = 11) and lesional and non-lesional skin of patients with diffuse (N = 5) and limited (N = 5) forms of SSc were obtained and serial sections prepared. Immunoperoxidase staining of these sections was carried out using four monoclonal antibodies (MoAbs) directed to different epitopes of DAF, four to different epitopes of MCP, one to CD59 and one to von Willebrand factor. von Willebrand factor served as a marker of endothelial cells. Besides normal skin, lesional skin of systemic lupus erythematosus and several inflammatory and proliferative diseases, described below, served as controls. RESULTS: The endothelium of normal skin strongly expressed all the three proteins. However, the endothelium of lesional and nonlesional skin of all the 10 patients with diffuse or limited forms of the disease tested, expressed either decreased or undetectable amounts of MCP and DAF. CD59 expression was normal in some patients and lower than normal in others. Aberrant expression of MCP, DAF, or CD59 was not found in other control inflammatory, connective tissue and proliferative diseases studied. CONCLUSIONS: In view of the common function of MCP and DAF to protect self cells from autologous C, their decrease or virtual absence from the endothelium of patients with SSc strongly suggests that this deficiency may contribute to vascular damage, resulting in intima proliferation and, finally, fibrosis.

Antibodies, Monoclonal↗
PubMed1994

Differential expression of ICAM-1, E-selectin and VCAM-1 by endothelial cells in psoriasis and contact dermatitis.

Adhesion receptors on endothelial cells are considered to be important for cellular influx in tissue. In this regard, skin constitutes a specialised environment for migration of leukocytes during inflammation. Using immuno-enzymatic staining techniques, we compared the in situ expression of ICAM-1, E-selectin, and VCAM-1 on endothelial cells and inflammatory infiltrates in both lesional and non-lesional biopsied skin from two immuno-inflammatory diseases, viz. psoriasis and contact dermatitis. The results were compared with those in skin specimens obtained from normal healthy individuals free from any history of skin disease. Our results show that ICAM-1 and ELAM-1 are upregulated in psoriatic non-lesional and lesional skin. On the other hand, in non-lesional biopsy from contact dermatitis patients, all three AR molecules are sparsely present, similar to the situation in normal skin although they are overtly expressed in the lesional sites. Moreover, VCAM-1 was found to be significantly increased on endothelial cells in the lesional sites of contact dermatitis as compared with biopsied psoriatic specimens. Interestingly VCAM-1 was also found to be present on some T-cells and Langerhans cells in contact dermatitis alone. The present data suggest that in different inflammatory dermatitis, varying adhesion receptor-ligand interactions involving endothelial cells and leukocytes are involved, which may be due to the differing cytokine profiles of perivascularly located T-cells.

Cell Adhesion Molecules↗
PubMed1994

Cellular interactions and adhesion molecules in psoriatic skin.

T-cell activation probably plays the most important role in hyperproliferation of keratinocytes in psoriasis. We present here our results concerning the interacting immunocompetent cells and their phenotypic and functional characteristics in relation to psoriasis pathology. Immunohistochemical analysis of skin biopsies from psoriasis patients, did indeed show that hyperproliferation of keratinocytes is associated with increased vasculature and increased influx of MHC class II molecules expressing immunocompetent cells. Furthermore, in psoriasis, several adhesion molecules and other relevant activation markers were found to be upregulated even in the non-lesional psoriatic skin, indicating that psoriatic skin in general is in an activated state. This interpretation is further supported by the observation that the expression of several AR and other relevant activation markers when compared with those in non-lesional skin from contact dermatitis are increased in a significant manner in the non-lesional skin of psoriasis patients. We have then followed up our investigations by generating T-cell lines from lesional psoriatic skin and studied their adhesion patterns on cultured endothelial cells in order to get better insight into the migration pattern of different T cell subsets in psoriasis pathology. Our results indicate that different T-cell subsets CD4+, CD8+ (both TCR-alpha beta+) CD4-/CD8+ TCR-gamma delta+ and CD4-CD8-TCR-gamma delta (V delta 1-) T-cells can easily be generated from psoriatic patients. In a comparative kinetic study using unstimulated and stimulated cultured human umbilical vein endothelial cells, we observed that TCR-gamma delta T cells showed different adhesion properties from that of TCR-alpha beta+ T cell subsets.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Adhesion↗
PubMed1994

Characterization of lesional psoriatic skin T lymphocyte clones.

T cells are considered to play a role in the pathomechanism of psoriasis. Therefore we investigated the cytokine production patterns of T cell clones that were randomly prepared from chronic plaque psoriasis lesions of 2 patients. 67% of the 49 T lymphocyte clones (TLC) expressed CD4 and 33% expressed CD8 (ratio 2:1), while gamma delta-TCR expression was absent. The production of IL-4, IFN-gamma, IL-2 and IL-6 was measured in supernatants of TLC following PHA plus PMA stimulation. Different groups of clones could be distinguished according to their IL-4/IFN-gamma production ratio. In addition to Th0 cells (low IL-4/low IFN-gamma), low IL-4/high IFN-gamma producers as well as high IL-4/low IFN-gamma producing clones were found, suggesting the presence of Th1- and Th2-like subsets. Upon stimulation, all TLC secreted low levels of IL-2 whereas a minority of the TLC secreted low levels of IL-6. These results may imply that T cells in psoriasis lesions do not show shifts towards either a Th1 or a Th2 cytokine production profile.

CD4-CD8 Ratio↗
PubMed1994

Functional evidence that the HECA-452 antigen is involved in the adhesion of human neutrophils and lymphocytes to tumour necrosis factor-alpha-stimulated endothelial cells.

The migration of leucocytes into tissues is a process mediated by leucocyte endothelial interactions, in which adhesion receptors play a crucial role. Recently, it was found that 80-90% of T cells in inflammatory skin diseases were reactive to the monoclonal antibody (mAb) HECA-452+ in contrast to inflamed non-cutaneous tissues. It was suggested that the HECA-452 antigen is a homing receptor for lymphocyte migration into skin. This receptor was designated cutaneous lymphocyte-associated antigen or CLA and subsequently identified as a group of related sugar moieties. E-selectin, formerly known as ELAM-1 expressed by the endothelium has been implicated to be a counter-receptor for CLA. In this study, we investigated the adhesion of HECA-452+ leucocytes, i.e. freshly isolated neutrophils and B-cell line BV173 to tumour necrosis factor-alpha (TNF-alpha)-stimulated (E-selectin+) endothelial cells. We found that the adhesion of these cells could be inhibited significantly by mAb HECA-452, in a similar fashion to CSLEX1, a mAb specific for E-selectin ligand sialyl Lewisx. This inhibiting effect of both mAb on the adhesion of polymorphonuclear leucocytes (PMN) and BV173 could only be demonstrated when the assay was performed at 4 degrees, but not at 37 degrees. Furthermore, using immunohistochemical analysis we found that the mAb HECA-452-reactive epitope is different from that recognized by CSLEX1. The present results give direct evidence that the antigen recognized by HECA-452 is involved in the adhesion of leucocytes to endothelial cells, although this antigenic epitope is different from that reactive to CSLEX1.

Antibodies, Monoclonal↗
PubMed1993

Prostaglandin E2 differentially modulates cytokine secretion profiles of human T helper lymphocytes.

PGE2 is a well known immunomodulator that has multiple effects on the immune system. We demonstrate that PGE2 selectively and dose dependently inhibits IL-2 and IFN-gamma production by mitogenically stimulated human PBL and CD4+ TLC, although at low concentrations IL-4 production is not affected and IL-5 production is even up-regulated. In the tested TLC, PGE2 induced a dramatic elevation (up to 85-fold) of the intracellular cAMP levels. The action of PGE2 may, therefore, be associated with elevation of intracellular cAMP levels, affecting IL-4 and IL-5 differentially from IL-2 and IFN-gamma production. To test this hypothesis we investigated cytokine production by TLC in the absence or presence of agents that affect cAMP levels, either directly (2'-O-dibutyrylcAMP) or through activation of adenylate cyclase (forskolin) or by blocking of phosphodiesterase (3-isobutyl-1-methyl-xanthine). Similar to PGE2, forskolin, 2'-O-dibutyrylcAMP, and 3-isobutyl-1-methyl-xanthine induced inhibition of IL-2 production by TLC and up-regulation of IL-5 production. However, in contrast to PGE2, these agents suppressed IL-4 production although IFN-gamma production was only moderately affected. No significant differences were found between intracellular cAMP levels of mitogenically stimulated Th1 cell clones, which predominantly secrete IL-2 and IFN-gamma, and those of Th2 cell clones, which mainly secrete IL-4 and IL-5. Our results indicate that PGE2 selectively modulates cytokine secretion profiles of human T cells and that elevation of cAMP levels has an important, but possibly not exclusive, regulatory role in this phenomenon.

Animals↗
PubMed1993

Serum-IgE-facilitated allergen presentation in atopic disease.

The occurrence of facilitated Ag presentation (FAP) was investigated in atopic disease using an in vitro model in which the ability of CD23-expressing EBV-B cells was tested to present Der p II, a major allergen of housedust mite Dermatophagoides pteronyssinus, to cells of autologous Der p II-specific CD4+ T lymphocyte clones. Purified Der p II protein was immune complexed with Ig by preincubation in sera from atopic patients containing Der p II-specific IgE. Incubation of EBV-B cells with these complexes before using the cells as APC results in proliferation of the Der p II-specific T cells at a 1000-fold lower Der p II concentration than required for T cell activation by presentation of uncomplexed Der p II. FAP is not evident using sera from allergic and nonallergic control donors not containing Der p II-specific IgE. FAP is mediated by IgE and not by IgG, because it can be blocked completely by preincubating the serum from atopics with polyclonal anti-IgE and not with polyclonal anti-IgG. After pulsing EBV-B with precomplexed Der p II at 4 degrees C, FAP is as strong as after incubation at 37 degrees C, suggesting that FAP is the result of facilitated trapping of IgE-complexed allergen. CD23 was involved in facilitated trapping of the complexes, because FAP is blocked by preincubation of EBV-B with anti-CD23. In contrast to FAP of Der p II, which was mediated by all Der p II-specific sera tested, only one of four sera containing cat allergen-specific IgE was appropriate to mediate FAP to cat allergen-specific T cell clones. Inasmuch as FAP enables functional presentation of allergen in vivo at doses as low as several nanograms, FAP may contribute to the continuing of chronic allergic reactions in response to minute doses of aeroallergens, especially housedust mite allergens, in the environment.

Allergens↗
PubMed1993

Skin-homing T lymphocytes: detection of cutaneous lymphocyte-associated antigen (CLA) by HECA-452 in normal human skin.

The immigration of circulating T cells into specific tissues is directed by the interaction between adhesion molecules on lymphocyte subpopulations and their ligands on vascular endothelium. Of these, endothelial leucocyte adhesion molecule (ELAM-1), weakly expressed in normal human skin (NHS), seems to be the counter-structure for cutaneous lymphocyte-associated antigen (CLA). CLA is a 200 kDa cell-surface glycoprotein of which the sugar moieties sialyl Le(a) and sialyl Le(x) are the possible epitopes recognized by the monoclonal antibody HECA-452. HECA-452 was originally described as a marker for lymphoid organ high endothelial cells, but 16% of peripheral-blood-derived T cells react with this antibody. We studied the expression of CLA on the cellular constituents of the skin immune system (SIS). By applying immunohistochemical double staining, 41% of CD3+ T cells, 44% of CD4+ T cells and 31% of CD8+ T cells were found to express CLA. Keratinocytes, CD1a+ Langerhans cells (LC) and endothelial cells did not express HECA-452 in significant numbers in NHS. Monocytes were found to express HECA-452 in 14% of CD68+ cells. CLA expression was present on a relatively low percentage of T cells and subsets localized distant from NHS vessels, suggesting loss of the molecule during further migration after transendothelial passage. However, intraepidermal T cells expressed CLA in similar percentages to T cells localized directly perivascularly. Our findings support the notion that CLA expression by T cells is associated with their homing into cutaneous structures.

Antibodies, Monoclonal↗
PubMed1993

The skin immune system: progress in cutaneous biology.

The skin is an active, and in many ways unique, immunological microenvironment quite different from the other primary interfaces between the body and the environment (namely the mucosae). Here Jan D. Bos and Martien L. Kapsenberg identify the components of the skin immune system and describe the inflammatory and immunological responses that they can mount. New findings with regard to the immunophysiology and physiopathology of the human integument are emphasized.

Autoimmune Diseases↗
PubMed1993

Antibodies to mycobacterial 65-kDa heat shock protein and other immunodominant antigens in patients with psoriasis.

An association of microbial agents and autoimmunity has been suggested for the pathogenesis of psoriasis. Mycobacteria are common environmental microbes and their antigens, especially the highly conserved mycobacterial 65-kDa heat shock protein (hps65), have been implicated in the pathogenesis of autoimmune arthritis and other idiopathic diseases. In this context, we investigated a possible mycobacterium-induced humoral immune response in psoriasis. Sera from 17 patients with chronic plaque-type psoriasis were studied by immunoblotting using the whole sonicate of Mycobacterium tuberculosis and purified recombinant mycobacterial hsp65. Immunoblot analysis demonstrated that 58% of the psoriasis patients compared to patients with acne and DLE, and normal controls showed strong antibody activity to 65-kDa and 48/45 doublet antigens from M. tuberculosis sonicate, whereas 47% of the patients showed antibody activity to mycobacterial hsp65. Only 10-20% of the patients had an antibody response to 16-kDa and 80-kDa antigens. Similar antibody activity to 65 kDa and 48/45 kDa was also found consistently with eight different sonicated mycobacterial species by immunoblotting, indicating that these seroreactive antigens are crossreactive and are present in common environmental mycobacteria. Antibody activities to both mycobacterial 65-kDa and hsp65 showed a positive correlation (r = 0.76) with the psoriasis disease activity, whereas antibodies to 48/45-kDa doublet antigens showed a weak correlation (r = 0.54). By enzyme-linked immunosorbent assay (ELISA), 47% of the psoriasis patients showed significantly elevated antibody titers to hsp65 (p < 0.003) as compared to control groups, and the antibody response by ELISA also showed a significant positive correlation (r = 0.76) with disease activity. Anti-mycobacterial antibody activity may be related to severity of disease and may be useful in monitoring disease activity in psoriasis.

Adult↗
PubMed1993

Effect of low-dose ultraviolet-B radiation on the function of human T lymphocytes in vitro.

Purified peripheral blood human T lymphocytes, derived from normal individuals, were assayed for their susceptibility to low doses of ultraviolet B (UVB) in vitro. Exposure of T cells to graded single doses (range 0-8 mJ/cm2) of UVB resulted in a dose-dependent reduction of viability. This phototoxic effect was not immediately apparent, however, but became manifest 48-72 h subsequent to irradiation. A dose as little as 0.5-1 mJ/cm2 was sufficient to cause 50% mortality. Irradiated T cells showed a reduced ability to proliferate, irrespective of the stimulus used, and a reduced ability to produce cytokines IL-2, IL-4, IL-5, interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha). This decreased ability was UVB-dose related and, remarkably, was exactly correlated to phototoxicity. UVB had no effect on CD4 and CD8 expression or their ratio, whereas the expression of IL-2R (CD25) was only slightly reduced. Our data suggest that UVB radiation neither selectively affects Th1 or Th2 nor CD4 or CD8 T cell subsets. The high susceptibility of T cells to UVB might explain, at least in part, the beneficial effect of phototherapy during treatment of certain immunodermatological diseases.

CD4 Antigens↗
PubMed1993

Review of the etiopathomechanism of vitiligo: a convergence theory.

Vitiligo is an acquired melanin pigmentary disorder manifesting itself by expanding depigmented lesions of the skin. To date, the etiopathomechanism of vitiligo has not been convincingly elucidated and a number of seemingly mutually opposed hypotheses with equal likelihood still coexist. Concurrent theories on vitiligo etiology, together with supportive evidence, are reviewed here. Due to the observed variation in clinical manifestations of the disease, it seems likely that the etiology of vitiligo may differ among patients. Therefore several theories on vitiligo etiopathogenesis have been combined to formulate a convergence theory for vitiligo, also presented in this article. This theory states that stress, accumulation of toxic compounds, infection, autoimmunity, mutations, altered cellular environment and impaired melanocyte migration and/or proliferation can all contribute to vitiligo etiopathogenesis in varying proportions.

Autoimmune Diseases↗
PubMed1992

Clinical evaluation of fifty-six patients referred with symptoms tentatively related to allergic contact stomatitis.

During a 7-year period, 56 patients were referred to the Department of General Pathology and Internal Medicine and the Department of Dental Materials, University of Amsterdam, to determine whether contact allergic reactions to dental materials were the cause of their complaints. On the first consultation with the patient a detailed history focusing on the complaints themselves, general medical history, and special clinical history of allergic skin reaction was obtained. Oral examinations were performed, and all patients were referred to the allergy clinic at the department of dermatology for skin tests. There was a strong female predominance in the referred group. Most of the patients with allergic contact stomatitis mentioned a burning sensation in the mouth. In only 16 of the 56 patients could the diagnosis of allergic contact stomatitis be established. From this study it can also be concluded that the combination of a positive allergic history and positive allergic skin reactions with or without visible oral signs are important for the diagnosis of allergic contact stomatitis.

Acrylic Resins↗
PubMed1992

Role of type 1 and type 2 T helper cells in allergic diseases.

Various characteristics of atopic allergic disorders seem to be causally related with the activation of allergen-specific T helper lymphocytes with a type 2 cytokine secretion profile, including high levels of interleukin-4 and interleukin-5. These cytokines are responsible for the occurrence of elevated levels of serum allergen-specific IgE and eosinophilia and play an important role in local inflammatory reactions.

Humans↗
PubMed1992

A comparison of the inhibitory effects of immunosuppressive agents cyclosporine, tetranactin, and didemnin B on human T cell responses in vitro.

The agents cyclosporine, tetranactin (TN), and didemnin B (DB) were compared for their ability to inhibit proliferative human T cell responses in vitro, using anti-CD3, PHA, alloantigen, or tetanus toxoid as stimuli and using monocytes or Langerhans cells as antigen-presenting cells/accessory cells (APC/AC). We found that all three agents suppressed T cell activation in a dose-dependent fashion, irrespective of the stimulus of APC/AC type used. Both T cells and APC/AC were affected by the drugs. DB appeared to be the most potent suppressive drug (IC50 = 1-4 ng/ml), whereas CsA and TN exerted approximately similar potency (IC50 = 50-60 ng/ml). Remarkably however, DB was toxic at a concentration of 10 ng/ml, which is quite close to the inhibition-inducing dose. No toxicity was observed with CsA and TN at doses up to 5000 ng/ml. The agents TN and DB could interrupt ongoing T cell responses and could block responsiveness to exogenous recombinant IL-2. Expression of IL-2 receptors was slightly inhibited by all three drugs. Expression of MHC class II molecule HLA-D and of adhesion molecules LFA-1, LFA-3, and ICAM-1 was clearly reduced by DB, giving an explanation for the observed inhibition of cluster formation between T cells and APC/AC. Except for a slight reduction of LFA-3 by TN, CsA and TN did not affect the expression of any of these cell surface markers or the formation of clusters. Differences in the effects of CsA, TN, and DB on immune responses in vitro and on the phenotype of T cells and APC/AC suggest that these immunosuppressive drugs have different inhibitory mechanisms.

Cell Survival↗