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Biomedical subjects

B Tank

Publications and source records attributed to B Tank.

At least 19 recordsLinked to original sources
PubMed2005

Mast cell distribution in normal adult skin.

AIMS: To investigate mast cell distribution in normal adult skin to provide a reference range for comparison with mastocytosis. METHODS: Mast cells (MCs) were counted in uninvolved skin adjacent to basal cell carcinomas and other dermatological disorders in adults. RESULTS: There was an uneven distribution of MCs in different body sites using the anti-tryptase monoclonal antibody technique. Numbers of MCs on the trunk, upper arm, and upper leg were similar, but were significantly different from those found on the lower leg and forearm. Two distinct groups were formed--proximal and distal. There were 77.0 MCs/mm2 at proximal body sites and 108.2 MCs/mm2 at distal sites. Adjusted for the adjacent diagnosis and age, this difference was consistent. The numbers of MCs in uninvolved skin adjacent to basal cell carcinomas and other dermatological disorders were not different from those in the control group. Differences in the numbers of MCs between the distal and the proximal body sites must be considered when MCs are counted for a reliable diagnosis of mastocytosis. A pilot study in patients with mastocytosis underlined the variation in the numbers of MCs in mastocytosis and normal skin, but showed a considerable overlap. The observed numbers of MCs in adults cannot be extrapolated to children. CONCLUSIONS: MC numbers varied significantly between proximal and distal body sites and these differences must be considered when MCs are counted for a reliable diagnosis of mastocytosis. There was a considerable overlap between the numbers of MCs in mastocytosis and normal skin.

Adolescent↗
PubMed2002

Urinary N-methylhistamine as an indicator of bone marrow involvement in mastocytosis.

Thirty-seven patients with mastocytosis and unexplained elevated levels of urinary N-methylhistamine who were undergoing bone marrow biopsy were studied with respect to the diagnosis of mastocytosis and the manifestations of the disease. These patients were from a group of 66 patients from whom a bone marrow biopsy was obtained and urinary N-methylhistamine levels were measured in the period 1990-1998. In seven (19%) of the 37 patients, mastocytosis was limited to the skin. Five (14%) of the 37 patients showed accumulation of mast cells in the bone marrow without characteristic skin lesions, whereas seven (19%) of the 37 patients showed increased numbers of mast cells both in the skin and the bone marrow. Eighteen (49%) of the 37 patients with elevated N-methylhistamine did not have mast cell accumulation in either the skin or the bone marrow biopsy. The median level of N-methylhistamine in the urine of patients with mastocytosis limited to the skin was 245 micro mol/mol creatinine. The average level of N-methylhistamine was 509 micro mol/mol creatinine in patients with mast cell accumulation in the bone marrow and cutaneous mastocytosis. There was a significant difference in the levels of N-methylhistamine in patients with mast cell accumulation in the bone marrow biopsy compared with those without. The likelihood of mastocytosis with mast cell accumulation in the bone marrow biopsy at a given level of N-methylhistamine was calculated. It was established that an N-methylhistamine level of 297 micro mol/mol creatinine or higher may be considered as a threshold indicator for obtaining a bone marrow biopsy in patients suspected of mastocytosis with mast cell accumulation in the bone marrow. For practical purposes, we propose to consider the cut-off level of approximately 300 micro mol/mol N-methylhistamine creatinine for this assay.

Biomarkers↗
PubMed2002

Comparison of mastocytosis with onset in children and adults.

OBJECTIVE: To compare the incidence, symptomatology and course of mastocytosis with onset in childhood and in adults. DESIGN: Retrospective study of 101 patients with mastocytosis who were referred from 1980 to 1998. PATIENTS: Medical records of 65 cases of mastocytosis with onset in childhood and 36 in adulthood were analysed. The clinical course was assessed in a subgroup consisting of 33 subjects with childhood onset who were followed up until at least adolescence and 12 subjects with adult onset who were followed up for at least 10 years. RESULTS: The onset of the disease occurred before the age of 2 years in 50% and between the ages of 2 and 15 years in 14% of cases (childhood onset). In 36% of patients onset occurred at the age of 16 years and older (adult onset). An incidence peak of 60% was noted in the first year of life. Mast cell-mediated symptoms were not experienced by 21 of 36 adult onset mastocytosis patients nor by 27 of 65 childhood onset mastocytosis patients. Complete resolution was observed in five of 33 children. The majority of childhood onset cases (21 of 33) showed some improvement. Complete resolution was achieved in three of 12 adults. The majority of the remaining adults (eight of 12) showed no improvement. CONCLUSIONS: We confirm the incidence of onset of mastocytosis previously reported in the literature. We conclude that childhood onset mastocytosis is much less transitory than generally is assumed, although improvement occurs in the majority of cases. Symptomatology and clinical course of adult onset mastocytosis is less severe than suggested in the literature.

Adolescent↗
PubMed1999

Interferon-gamma-induced ICAM-1 and CD40 expression, complete lack of HLA-DR and CD80 (B7.1), and inconsistent HLA-ABC expression in basal cell carcinoma: a possible role for interleukin-10?

Basal cell carcinomas (BCCs) of the skin show varying degrees of peritumoural inflammatory infiltrate consisting mainly of T cells, but lack an effective T-cell-mediated immune response. This may be caused by the absence of the major histocompatibility complex (MHC) class I and II antigens, intercellular adhesion molecule-1 (ICAM-1), CD40 and CD80 (B7.1). Interferon-gamma (IFN-gamma) is known to induce or up-regulate their expression on epithelial cells, whereas interleukin-10 (IL-10) down-regulates their expression. The induction and up-regulation of HLA-ABC, HLA-DR, ICAM-1, CD40, and CD80 in BCC and normal skin from BCC patients were investigated in a culture system using recombinant human IFN-gamma (rHuIFN-gamma). The levels of IL-10 were determined in the supernatants after culture. The results showed that only ICAM-1 expression was significantly up-regulated on BCC cells. However, in the normal epidermis of BCC patients and in the epidermis overlying the tumour nests, significant up-regulation of ICAM-1, and CD40, and CD80 and slight up-regulation of HLA-DR were observed. No changes in HLA-ABC expression were observed in either normal skin or BCC. High levels of IL-10 were present in the supernatants of BCC biopsies after culture. It may be concluded that it is highly likely that the presence of IL-10 in BCC is directly or indirectly responsible for the complete lack of expression of HLA-DR, ICAM-1, CD40 and CD80 and the inconsistent expression of HLA-ABC on BCC cells in situ and may be a way of escaping immune survillance.

Adult↗
PubMed1999

Expression of E-cadherin, alpha- & beta-catenin, and CD44V6 and the subcellular localization of E-cadherin and CD44V6 in normal epidermis and basal cell carcinoma.

Basal cell carcinoma (BCC) of the skin is a locally invasive, rarely metastasizing epithelial tumor. In the current study, the expression of E-cadherin, alpha- and beta-catenin and CD44V6 in normal epidermis and on BCC cells were investigated. A significantly reduced expression of alpha-catenin and CD44V6 and a slightly reduced expression of E-cadherin on BCC cells were observed compared with the overlying epidermis. Immunoelectron microscopy was used to investigate whether the decreased expression of E-cadherin and CD44V6 was due to either an absence or downregulation of specific membrane structures or due to an overall downregulation of these adhesion molecules in all membrane structures in BCC. E-cadherin and CD44V6 were expressed in adherens junctions, desmosomes, and complex interdigitating membrane structures both in normal epidermis and in BCC. A quantitative analysis showed that only a percentage of desmosomes was stained. In addition, the effect of pro-inflammatory cytokines, such as interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), was investigated in biopsy specimens of normal skin and BCC, using a biopsy culture system and immunohistochemistry. The expression of E-cadherin and CD44V6 was not significantly decreased after culturing BCC or normal skin biopsy specimens for 48 hours with or without recombinant human (rHu)IFN-gamma or rHuTNF-alpha. It may be concluded that the decreased expression of both E-cadherin and CD44V6, observed in light microscopy, was not attributable to the absence of specific specialized structures in BCC and most likely also not caused by downregulation by local cytokines, but rather by generic downregulation of both of these adhesion molecules during malignant transformation.

Aged↗
PubMed1998

Expression of interferon-gamma receptors and interferon-gamma-induced up-regulation of intercellular adhesion molecule-1 in basal cell carcinoma; decreased expression of IFN-gamma R and shedding of ICAM-1 as a means to escape immune surveillance.

The peritumoural inflammatory infiltrate in basal cell carcinoma (BCC) of the skin consists mainly of T lymphocytes which hardly invade the tumour nests. The absence of intercellular adhesion molecule-1 (ICAM-1) on BCC cells may explain the lack of tumour-infiltrating cells and the lack of an active cell-mediated immune response in this tumour. In this study, the induction of ICAM-1 was investigated in BCC biopsies using recombinant human interferon-gamma (rHuIFN-gamma). The expression of interferon-gamma receptors (IFN-gamma R) in the biopsies was also investigated. The results showed that BCC cells expressed ICAM-1 after incubation with rHuIFN-gamma, but to a lesser degree than normal epidermal cells. The levels of shed ICAM-1 were significantly increased in the culture supernatants of tumour biopsies compared with those from normal skin biopsies, after culturing in the presence of rHuIFN-gamma. The expression of IFN-gamma R was significantly decreased on the tumour cells compared with the overlying epidermis. The decreased expression of IFN-gamma R on the tumour cells and the shedding of ICAM-1 into the peritumoural stroma may be a plausible mechanism by which the tumour cells are protected against an active cell-mediated immune response.

Adult↗
PubMed1996

Adhesion molecules and IL-1 costimulate T lymphocytes in the autologous MECLR in psoriasis.

Membrane molecules such as CD36 (OKM5), intercellular adhesion molecule-1 (ICAM-1, CD54), gamma interferon-induced protein 10 (gamma-IP10) and IL-1 are induced and/or upregulated in psoriatic epidermis. These molecules have important accessory, trafficking or signalling functions in the immune system and also play a role in the pathophysiology of psoriasis. The relevance of adhesion molecules, CD36 and epidermal IL-1 in psoriasis was studied in vitro in the autologous mixed epidermal cell - T lymphocyte reaction (MECLR). Their level of expression was quantitated in epidermal cell suspensions (ECS) from patients with psoriasis and their function was assessed by blocking with specific mAbs and antisera or by depleting CD36+ cells from the ECS prior to the MECLR. ECS from psoriatic lesions contained increased numbers of CD36+ (23 +/- 12%), ICAM-1(+) (31 +/- 14%) and IL-1(+) (57 +/- 21%) cells. The autologous MECLR was inhibited in samples from all patients by mAb to CD2 (LFA-2), CD11a (LFA-1alpha), CD18 (LFA-1beta), ICAM-1, CD58 (LFA-3) and an antiserum to IL-1beta. Thus, adhesion molecules facilitate inflammation in psoriasis not only via adhesion and recruitment of T lymphocyte in psoriatic lesions, but also via activation of T cells. Furthermore CD36 molecules on psoriatic epidermal cells do not costimulate autologous T lymphocytes in psoriasis. The observed costimulatory function of IL-1beta in the MECLR emphasizes its relevance in psoriasis.

Antibodies, Monoclonal↗
PubMed1992

Cyclosporine in atopic dermatitis. Modulation in the expression of immunologic markers in lesional skin.

BACKGROUND: In previous studies, oral cyclosporine was highly effective in the treatment of patients with severe atopic dermatitis. In this study seven patients with severe and therapy-resistant atopic dermatitis underwent therapy with cyclosporine, 5 mg/kg/day, for 6 weeks. OBJECTIVE: The effect of cyclosporine on the expression of cytokines, which probably play a role in this disease, was examined. METHODS: The study was performed with a panel of antibodies as markers of inflammatory cells, adhesion molecules, and cytokines (interferon-gamma [IFN-gamma], tumor necrosis factor-alpha [TNF-alpha] and interleukins 1 alpha, 1 beta, and 8 [IL-1 alpha, IL-1 beta, and IL-8, respectively]). They were visualized by indirect immunoperoxidase techniques. RESULTS: After 2 weeks of cyclosporine therapy, a reduction of 60% in the disease (severity and extent) was observed. This reduction was 89% after 4 weeks and 90% after 6 weeks of therapy. Results of indirect immunoperoxidase stains performed on lesional skin sections after 2 weeks of treatment showed statistically significant reduced numbers of CD14+, CD25 (IL-2R+) and IL-8+ inflammatory cells in the dermis and CD36(OKM5)+ cells in both the epidermis and dermis. The number of cells expressing IFN-gamma and TNF-alpha, assumed to be the products of the helper T-cell (TH)1 subset, was unaltered despite the impressive clinical benefit observed. Keratinocytes in lesional atopic skin did not express intercellular adhesion molecule type 1 (ICAM-1). The expression of the adhesion molecules ICAM-1, lymphocyte function-associated (LFA) type 1, and LFA-3 on inflammatory cells also remained unaffected by cyclosporine treatment. CONCLUSION: A statistically significant reduction in the number of activated T cells and in the number of cells expressing the IL-2 receptor (CD25) paralleled a marked improvement in the disease and supports the view that atopic dermatitis is based on a T-cell-mediated immune inflammation.

Administration, Oral↗
PubMed1991

Benign persistent papular acantholytic and dyskeratotic eruption: a case report and review of the literature.

We report a case of a 35-year-old female with a persistent pruritic acantholytic and dyskeratotic eruption on the chest and vulva. The light and electron microscopic studies showed suprabasal epidermal clefting with acantholysis and dyskeratotic cells. We suggest that the most appropriate term for this case is that of benign persistent papular acantholytic and dyskeratotic eruption.

Adult↗
PubMed1990

Purpuric contact dermatitis to benzoyl peroxide.

Patch test reactions in a patient with purpuric contact dermatitis to 5% benzoyl peroxide are described. Alterations of the capillary endothelium included obliteration of the lumina with perivascular mononuclear cell infiltrates. There were no epidermal alterations. These observations are discussed with reference to the data in the literature on vascular damage in "dermal" contact dermatitis.

Adult↗
PubMed1989

Optimizing the solid-phase immunofiltration assay. A rapid alternative to immunoassays.

The technical variables of the solid-phase immunofiltration assay (SPIA) for the detection of antibodies bound to antigens on a solid-phase filter have been investigated. The binding to solid-phase filters of 125I-labelled axial filament proteins derived from Treponema phagedenis and the optimal conditions for blocking non-specific protein binding were analysed. Axial filament was applied to nitrocellulose, Hybond Nylon and Zeta Probe. After extensive rinsing, the highest amount (68%) of axial filament was observed bound to Zeta Probe. However, blocking non-specific protein binding by pre-wetting the filter with rinsing buffer containing 0.5% Tween 20, prevented the binding of protein to the filter only when nitrocellulose was used as solid phase. Tween 20 (0.5%) in the rinsing and incubation solutions was found to be necessary for the reduction of non-specific binding of contaminants in turbid sera. However, the use of such solutions resulted in a substantial leakage of antigen (47%) during rinsing procedures. Binding of antigen-specific antibody was analysed using 125I-labelled protein A. The maximal possible binding of the antibody occurred within 5 min when the antibody solution was filtered. For optimal binding of 125I-labelled protein A an incubation time of 1 h was needed. It is suggested that solid-phase immunofiltration may provide a rapid alternative for radioimmunoassays or enzyme immunoassays for the detection of specific antibodies.

Animals↗
PubMed1989

Characterization of the mononuclear infiltrate in Bowen's disease (squamous cell carcinoma in situ). Evidence for a T cell-mediated anti-tumour immune response.

We investigated the dermal inflammatory infiltrate and the expression of HLA-DR and beta 2-microglobulin on the tumour cells in 8 Bowen's disease (BD) using a series of monoclonal antibodies. The inflammatory infiltrate was classified as mild, moderate or heavy. The infiltrate in all cases consisted mainly of T cells (55 +/- 21%) and where the T helper (TH) subset predominated over the T suppressor/cytotoxic (TS/C) subset (TH/TS/C ratio of 2.4 +/- 1.0). The mean percentage of HLA-DR positive cells was 58 +/- 18%, Langerhans cells (LC) 4 +/- 1% and Leu-M5 positive cells (monocytes/macrophages) 9 +/- 2%. The mean percentage of B cells and natural killer (NK) cells was 4 +/- 5% and 1 +/- 2% respectively. B cells and NK cells did not invade any of the tumours. In the 5 BD with moderate or heavy infiltrate, TH cells, TS/C cells and Leu-M5 positive cells did invade the tumour. In the tumour area where there was invasion, the number of LC was increased and HLA-DR was expressed on the cells. beta 2-microglobulin was generally expressed on the tumour cells of BD. We concluded that there is evidence for a T cell-mediated anti-tumour immune response which may account for the infrequent invasive growth in BD.

Adult↗
PubMed1989

Line immunoassay and enzyme-linked line immunofiltration assay for simultaneous detection of antibody to two treponemal antigens.

Two enzyme immunoassays, the line immunoassay (LIA) and the enzyme-linked line immunofiltration assay (ELLIFA), were studied for suitability in the serodiagnosis of syphilis. In both assays, antibody to treponemes was detected using the recombinant DNA derived treponemal protein TmpA and the purified axial filament derived from the Reiter treponeme. The antigens were applied in parallel lines onto nitrocellulose membranes. The sensitivity and specificity of both assays were compared with that of the Treponema pallidum hemagglutination assay (TPHA), the fluorescent treponemal antibody absorption test, and the axial filament and TmpA enzyme-linked immunosorbent assays. The sensitivity and specificity of the LIA and the ELLIFA were found to be comparable to that of the TPHA using serum samples from 65 untreated syphilitic patients, 95 patients treated for syphilis and 60 blood donors, except in the case of the LIA using axial filament. This latter test was slightly less sensitive in primary and early latent syphilis than the TPHA. In the LIA procedure, serum antibodies to two antigens could be detected simultaneously within two hours. This assay may be useful for fieldwork. In the ELLIFA procedure, antibodies to the two antigens could be detected simultaneously within 15 minutes. The ELLIFA procedure may provide a multiple antigen test with a very short assay operation time.

Antibodies, Bacterial↗
PubMed1989

An absence of human leukocyte antigen-DR and a decreased expression of beta 2-microglobulin on tumor cells of basal cell carcinoma: no influence on the peritumoral immune infiltrate.

The expression of human leukocyte antigen-DR (HLA-DR) and beta 2-microglobulin on the tumor cells and their correlation (if any) to the degree and the composition of the peritumoral mononuclear infiltrate were studied in 37 basal cell carcinomas from 32 patients with an indirect immunoperoxidase technique. In 36 of 37 basal cell carcinomas (97%) there was no expression of HLA-DR on tumor cells of basal cell carcinoma. In 13 of 37 basal cell carcinomas (35%) beta 2-microglobulin was expressed on the tumor cells. Both a diffuse cytoplasmic and a membrane staining were observed in only six of these 13 basal a diffuse cytoplasmic and a membrane staining were observed in only six of these 13 basal cell carcinomas; in the other seven basal cell carcinomas only a diffuse cytoplasmic staining was observed. In all 37 basal cell carcinomas there was membrane staining for beta 2-microglobulin in the normal epidermis. The intensity of staining in the normal epidermis was always stronger than that in the tumor nests. There was a varying degree of peritumoral immune infiltrate in all basal cell carcinomas. It comprised mainly T cells (mean percentage 57 +/- 15). In the group of patients with basal cell carcinoma with moderate to heavy infiltrate the mean percentage of T cells was 63 +/- 13, which was significantly higher than the mean percentage of T cells (46% +/- 14%) in the group of patients with basal cell carcinoma with a mild infiltrate. This difference was mainly the result of an increase in T helper cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Localized bullous pemphigoid, a T cell-mediated disease? Electron microscopic and immunologic studies.

Two new cases of the rare, nonmucosal and nonscarring localized variety of pemphigoid are described. With reference to the data in the recent literature, the disease was classified as Localized Bullous Pemphigoid (LBP). The ultrastructural and immunologic findings are described and are briefly discussed in the context of the possible mechanisms leading to local subepidermal tissue injury in LBP. Although classical features of humoral responsiveness (in vivo bound IgG and complement at the epidermal basal membrane-zone (BM-zone)) were observed, a possible additional role of T cell mediated immunity in generating this local disease is considered.

Aged↗