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The association of dermatitis herpetiformis (DH) with granular IgA deposits at the dermal-epidermal junction and a gluten sensitive enteropathy (GSE) suggests that a mucosal immune response may play an important role in the pathogenesis of DH. The degree of antigenic restriction, the immunoglobulin class and subclass response to dietary antigens, and the relationship of antibodies against dietary antigens to IgA-containing circulating immune complexes (CIC) in patients with DH, however, are not known. We have examined the serum of 33 patients with DH for IgG and IgA antibodies against gliadin, and against 3 dietary proteins not thought to be related to GSE, beta-lactoglobulin (beta-lacto), bovine gamma globulin (BGG), and casein. Eleven of 33 (33%) patients with DH had IgA anti-gliadin antibodies, whereas IgA antibodies against beta-lacto were found in 11 of 33 patients (33%), against BGG in 15 of 32 (47%), and against casein in 6 of 33 (18%); 17 of 32 (53%) patients had IgA antibodies against one or more of these dietary antigens. Significantly higher levels of IgA antibodies were detected against beta-lacto (2,500 +/- 2,320 ng/ml, mean +/- SEM) and BGG (2,340 +/- 1,890 ng/ml) than gliadin (1,250 +/- 851 ng/ml) in this group of antibody positive patients (p less than 0.05, Wilcoxon signed ranks test). Eleven of 17 patients with IgA antibodies against dietary antigens were found to have IgA-containing CIC, whereas only one of the 15 antibody negative patients had IgA-containing CIC (p = 0.0008, Fisher's exact test). IgA anti-gliadin antibodies were found to contain both IgA1 and IgA2 with a significantly increased proportion of IgA2 when compared with the IgA2 composition of the total serum IgA (IgA2: anti-gliadin antibodies = 34 +/- 4.2%; total serum IgA = 19 +/- 4.8%, p = 0.02, Students paired t test). IgG antibodies against these antigens were found to occur slightly more frequently in amounts not significantly greater than IgA antibodies. This data demonstrates that a serum IgA and IgG antibody response to dietary antigens occurs in approximately 50% of DH patients with a higher proportion of IgA2 than total serum IgA and does not appear to be restricted to gliadin. This is significantly different from the pattern of cutaneous immunoreactants in patients with DH, and suggests that the deposition of IgA in DH skin may be the result of an atypical mucosal immune response, a non-immunologic interaction of IgA1 and DH skin, or arise from a non-mucosal source.
J Invest Dermatol 1988 May
PMID:Characterization of the mucosal immune response to dietary antigens in patients with dermatitis herpetiformis. 325 98

Sclerosing or morphea-like variant of basal cell carcinoma (BCC) is characterized by an extensive connective tissue stroma, and histopathology has suggested that the extracellular matrix is largely composed of collagen. In addition, fibronectin deposition has been proposed to modulate tumor growth in BCC. In this study, we examined the expression of genes coding for type I, III, and IV procollagens, as well as for fibronectin, in tissue from 10 patients with sclerosing BCC. For comparison, tissues from 5 patients with nodular BCC and 4 controls were examined. Total RNA was isolated by CsCl density gradient centrifugation, and messenger RNA (mRNA) steady-state levels were determined by slot-blot hybridizations with human sequence specific complementary DNAs (cDNAs). The abundance of type I procollagen mRNA in sclerosing BCC tissue was increased to 233.6 +/- 36.7% of the controls (mean +/- SEM). The corresponding value for type III procollagen mRNA in sclerosing BCC was 281.8 +/- 54.8% of the controls. Consequently, the steady-state ratio of type I/III procollagen mRNAs in sclerosing BCCs (5.0 +/- 1.2; mean +/- SD) was within the control range. Thus, there is a coordinate increase in type I and type III procollagen mRNA levels in sclerosing BCC. In contrast, the values for type I and type III procollagen mRNAs in nodular BCC were not different from the controls. In addition, type IV procollagen and fibronectin mRNA levels were not different from the controls either in sclerosing or nodular BCCs, attesting to the selectivity of the increase in type I and III procollagen mRNA levels in sclerosing BCC. These observations may relate to the excessive deposition of the extracellular matrix stroma surrounding the tumor cells in sclerosing BCC.
J Invest Dermatol 1988 May
PMID:Selectively enhanced procollagen gene expression in sclerosing (morphea-like) basal cell carcinoma as reflected by elevated pro alpha 1(I) and pro alpha 1(III) procollagen messenger RNA steady-state levels. 336 Nov 39

The brown pigmentation of the skin associated with venous ulceration is caused by increased local iron deposition. Diagnostic x-ray spectrometry, a method based on x-ray fluorescence analysis, was used for the noninvasive determination of iron levels in the skin of patients with venous ulceration. The mean (+/- SEM) iron concentration in the skin around the venous ulcer was elevated, compared with control values of nonulcerated skin (250 +/- 54 vs 128 +/- 39 micrograms) and compared with normal skin from the forearm (250 +/- 54 vs 14 +/- 2.5 micrograms). These data suggest that dermal iron deposition may not be an incidental by-product of increased venous pressure, but may actively perpetuate tissue damage in venous ulcerations.
Arch Dermatol 1988 Sep
PMID:Overload of iron in the skin of patients with varicose ulcers. Possible contributing role of iron accumulation in progression of the disease. 341 80

In order to evaluate mast cell participation in allergic contact hypersensitivity (ACH), BALB/c mice were sensitized with 0.1% trinitrochlorobenzene (TNCB). Immediately before challenge and at 1, 1.5, 2, 4, 6, 8, 12, 24, and 48 h after challenge with 1% TNCB, groups of animals had ear thickness measured, had blood collected for histamine determinations, and had both ears removed for histologic evaluation of mast cells. The increase in ear swelling was triphasic with peak increases at 1.5 h (14.3 +/- 1.6 X 10(-2) mm; mean +/- SEM), 8 h (19.9 +/- 1.8 X 10(-2) mm), and 24 h (30.2 +/- 2.9 X 10(-2) mm). A triphasic pattern of increased serum histamine was noted at 1-4 h (117% over control levels), at 12 h (131%), and at 48 h (133%). Examination of the tissue specimens from challenged animals showed modest (1+) degranulation of mast cells between 1 and 6 h with extensive (2+) degranulation at 12 h. In addition, hypogranulated mast cells were evident between 1 and 6 h, at 24 h, and at 48 h. There were no statistically significant differences in mast cell numbers at any time. Neither platelets nor other formed elements of the blood contributed to the increased blood histamine levels. These data show that mast cells are activated in a triphasic pattern during ACH, and thus suggest both early and late roles for the mast cell and its products in the evolution of ACH.
J Invest Dermatol 1987 Jun
PMID:Mast cell participation during the elicitation of murine allergic contact hypersensitivity. 358 52

Non-Langerhans cell, antigen-presenting T6- DR+ epidermal cells (EC) appear 3 days following broad band ultraviolet radiation exposure of human skin and are responsible for the increased antigen presentation capacity of EC seen 3 days after UV exposure. To determine the UV wavelengths that induce T6- DR+ EC, volar forearm skin of 10 human volunteers was irradiated in vivo with 4 minimal erythema doses (MED) each of pure UVA (mean 482 J cm-2), UVB (mean 0.390 J cm-2), and UVC (mean 0.397 J cm-2). The purity of the light sources was as follows: UVB, 98% of the emission was in the UVB range; UVC, 97% of the irradiance was in the UVC range; UVA, 100% of the energy had wavelengths longer than 340 nm. Three days after UV irradiation with 4 MED of each wavelength band, suction blister-derived EC suspensions were prepared from the UV-exposed and unirradiated sites. Percentages of T6+ DR+ Langerhans cells (LC) and T6- DR+ EC were quantitated. Relative to control EC, which contained 2.4 +/- 0.3% T6+ DR+ LC, the mean percentage (+/- SEM) of T6+ DR+ LC contained within UV-exposed EC was significantly decreased as follows: UVB, 0.5 +/- 0.2%; UVC, 0.9 +/- 0.1%; UVA, 0.5 +/- 0.2% (n = 10). T6- DR+ EC, absent in control EC, were induced both by UVB, 5.2 +/- 1.7% and UVC; 1.5 +/- 0.4%. Despite the use of more than 1200 times greater doses in J cm-2 of UVA than UVB and UVC, UVA was a poor inducer of T6- DR+ EC (0.5 +/- 0.2%) and in about half of these individuals, T6- DR+ EC were undetectable. The UV wavelengths for induction of T6- DR+ EC lies predominantly within the UVB band, but also to a lesser extent within the UVC band. These wavelengths appear to be analogous to both the wavelengths for generation of increased host susceptibility to UV-induced murine tumors and to the wavelengths for UV-induced systemic suppression of contact hypersensitivity. However, our data indicate that UV wavelengths for decreasing the number of T6+ DR+ LC in humans differs from the wavelengths for induction of systemic suppression of contact hypersensitivity in mice. Taken together, these data suggest that the appearance of T6- DR+ EC, but not the disappearance of T6+ DR+ LC, following UV exposure may be related to the induction of such antigen-specific suppressor T cells.
J Invest Dermatol 1987 Jul
PMID:UVB and UVC, but not UVA, potently induce the appearance of T6- DR+ antigen-presenting cells in human epidermis. 359 1

Cutaneous mast cells from 3 patients with mastocytosis were evaluated for their morphologic characteristics and in vitro functional reactivities to different secretory agonists. By electron microscopy, mastocytosis mast cells appeared larger than normal skin mast cells, frequently had atypical, highly indented or bilobed nuclei, and each contained numerous, elongated cytoplasmic projections. Suspensions of mastocytosis mast cells were obtained from lesional skin biopsy specimens, and their response to both immunologic and nonimmunologic secretagogues was compared with mast cells from normal skin. Lesional skin mast cells had a net histamine release of 12.3% (+/- 1.3 SEM) and 31.1% (+/- 6.0 SEM) following stimulation with the purified human anaphylotoxin C3a and mouse monoclonal antihuman IgE antibodies, respectively. This specific release was similar to the responses observed in normal skin mast cells (11.5% +/- 4.5 SEM and 16.7% +/- 2.1 SEM, respectively). Mast cells from cutaneous lesions of mastocytosis also responded to the nonimmunologic secretagogues, morphine sulfate and calcium ionophore A23187 with a specific histamine release of 15.1% (+/- 1.2 SEM) and 39.8% (+/- 8.7 SEM), respectively. The results of this study demonstrate that mast cells from lesions of mastocytosis are morphologically atypical, but have a histamine content similar to normal skin mast cells and retain their functional reactivities to clinically relevant secretory stimuli.
J Invest Dermatol 1987 Sep
PMID:In vitro functional reactivities of cutaneous mast cells from patients with mastocytosis. 362 98

This study was designed to assess the role of the mast cell in the early phase of hematoporphyrin derivative (HPD)-induced phototoxicity. BALB/c mice were rendered phototoxic by i.p. injection of hematoporphyrin derivative, followed by exposure to 13.6 kJ/m2 of 400-410 nm radiation. The phototoxic response was quantified by measurement of ear thickness immediately before the irradiation, and at 0, 0.5, 1, 1.5, and 2 h after. At these time-points, determinations of serum histamine and plasma leukotriene C4 levels and histologic examination of the ears were undertaken. Mice injected i.p. with buffered saline and subsequently irradiated served as controls. In mice exposed to HPD and radiation, a maximal peak increased ear-thickness of 125.7 +/- 14.4% (mean +/- SEM) was noted at 2 h; this was associated with a net increased serum histamine of over 120% and histologic evidence of mast cell degranulation. In addition, moderate increases in plasma levels of leukotriene C4 were observed at 0 h and 1.5 h in the HPD- and irradiation-treated animals. These data provide direct evidence for the participation of mast cells in the early phase of HPD-induced phototoxicity.
J Invest Dermatol 1987 Mar
PMID:In vivo mediator release and degranulation of mast cells in hematoporphyrin derivative-induced phototoxicity in mice. 381 68

We determined the histamine content in the skin of 22 adults with atopic dermatitis, one patient with hyper-IgE-syndrome, and 20 controls by the enzymatic double isotope assay. In addition, we performed a pilot study of histamine degradation in the skin. We tested, furthermore, the releasability of histamine from skin sections of patients with atopic dermatitis and healthy controls upon challenge with acetylcholine, anti-IgE, and compound 48/80. Histamine was also determined in 13 plasma specimens and was always less than 1 ng/ml. The mean +/- SEM histamine concentration in the skin was 196 +/- 30 ng/mg protein in controls and 262 +/- 68 ng/mg protein in atopic dermatitis (no statistically significant difference). One control and three patients with atopic dermatitis exhibited a slight, the hyper-IgE patient a marked, elevation of the skin histamine content. No gross differences in the degradation rate of histamine were observed between patients and controls. Acetylcholine and 48/80 induced the same histamine release in both groups; with anti-IgE, almost the double amount of histamine was released from the skin of atopic dermatitis patients as compared to controls. These findings suggest an enhanced releasability of histamine upon immunologic challenge in atopic dermatitis.
Arch Dermatol Res 1983
PMID:Cutaneous histamine levels and histamine releasability from the skin in atopic dermatitis and hyper-IgE-syndrome. 618 56

Normal individuals who possess the HLA B8/DRw3 haplotype as well as patients with dermatitis herpetiformis have been found to have a number of immunologic abnormalities including decreased numbers of E rosette-positive, Fc IgG receptor-bearing lymphocytes (referred to as TG cells), and increased numbers of cells which spontaneously secrete immunoglobulin. HLA B8/DRw3-positive normal individuals also have an increased risk for the development of a number of immunologically mediated diseases. Since many of these findings are suggestive of B-cell hyperreactivity and since TG cells were initially thought to represent a portion of the T suppressor cell network, we have examined the peripheral blood mononuclear (PBM) cell populations of 14 normal HLA B8/DRw3-positive individuals, 14 patients with dermatitis herpetiformis (all of whom were HLA B8/DRw3-positive), and 9 non-HLA B8/DRw3 individuals using flow cytometry and monoclonal antibodies of the OK and Leu series directed against cell surface antigens. Normal HLA B8/DRw3 individuals were found to have a significantly lower percentage of PBM cells that expressed both OKT8 and Leu-2a when compared to normal non-HLA B8/DRw3 individuals (p less than .05 Student's t-test). When the ratio of T helper cells (OKT4 and Leu-3a) to T suppressor cells (OKT8 and Leu-2a) was calculated for each individual studied, normal HLA B8/DRw3 individuals were found to have a significantly elevated ratio (Leu-3a/Leu-2a = 2.41 +/- .16, mean +/- SEM) when compared to non-HLA selected individuals (Leu-3a/Leu-2a = 1.73 +/- .05) (p less than 0.025). In addition, normal HLA B8/DRw3 individuals had decreased numbers of TG cells when compared to normal non-HLA B8/DRw3 individuals (B8/DRw3 = 6.4 +/- .74%, non-B8/DRw3 = 13.2 +/- 1.0%, mean +/- SEM, p less than .01). In order to determine the cell surface marker characteristics of TG cells, purified TG cells from both normal HLA B8/DRw3 individuals and non-HLA B8/DRw3 individuals were studied using the Leu series monoclonal antibodies and OKM1. Good agreement was found in the percentages of cells expressing each cell surface marker between the two groups. In addition, the TG cells were found to be predominately T cells (78% Leu-1-positive), with both T helper cells (40% Leu-3a-positive) and T suppressor cells (30% Leu-2a-positive) present. These results suggest that the suppressor cell activity associated with the TG subset is not due to a depletion of the T helper cell subset, and that the decreased numbers of TG cells in HLA B8/DRw3 individuals is not due to a preferential loss of cells bearing Leu-1, Leu-2a, Leu-3a, or OKM1.(ABSTRACT TRUNCATED AT 400 WORDS)
J Invest Dermatol 1984 Mar
PMID:Characterization of T lymphocyte and monocyte populations in HLA B8/DRw3 normal individuals and in patients with dermatitis herpetiformis. 623 Apr 5

This paper reports the first case of skin metastases from small-cell carcinoma of the lung with electron microscopic confirmation. The 2 to 3-cm cutaneous lesions present on the chest and limbs were hard, nontender, smooth-surfaced, freely moveable nodules with normal appearing overlying skin. Characteristic dense-core granules 1562 +/- 123 A (SEM) in diameter were detected by electron microscopy. The detection by electron microscopy of dense-core granules may assist in confirming the diagnosis of small-cell carcinoma in cutaneous lesions with equivocal histologic findings.
J Dermatol Surg Oncol 1983 Jun
PMID:Skin metastases from small-cell carcinoma of the lung. 630 67


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