Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06126 (CD1a)
 2,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown that barrier requirements regulate epidermal liquid and DNA synthesis. In the present study, we examined the possibility that the integrity of the permeability barrier influences epidermal Langerhans cells involved with the immune response. Barrier disruption was achieved by treatment of human skin with acetone, sodium dodecylsulphate (SDS), or tape stripping, until a 10-20-fold increase in transepidermal water loss was achieved. Serial biopsies were performed 6-168 h after treatment, and Langerhans cells were complexed with anti-CD1a (Leu6) or S-100 antibodies, and visualized with an immunoperoxidase technique. Acetone treatment resulted in an increase in epidermal Langerhans cell density, reaching a maximum of 94% over control (P < 0.01) by 24 and 48 h post-treatment. Following SDS treatment or tape stripping, epidermal Langerhans cell density was increased by 100 and 175% (P < 0.01), respectively. There was a linear correlation between the degree of barrier disruption and the increase in epidermal Langerhans cell density. Studies with the Ki-S3 proliferation-associated nuclear antigen revealed a two- to threefold increase in epidermal proliferation after barrier disruption. The time curves of the increase in Langerhans cell density and the increase in epidermal proliferation were similar, suggesting that there was a coordinate regulation. In contrast with our previous studies employing patch test reactions to allergens or irritants, disruption of barrier function neither resulted in an increased dermal Langerhans cell density, nor influenced T lymphocytes (CD3+, Leu4+), macrophages (KiM8+), ICAM-1 or ELAM-1 expression in the skin. In addition, barrier disruption did not result in either dermal inflammation or epidermal spongiosis. In summary, these findings support our hypothesis that the permeability barrier influences epidermal Langerhans cell density, which is involved in maintaining an immunological barrier.
Br J Dermatol 1996 Apr
PMID:Integrity of the permeability barrier regulates epidermal Langerhans cell density. 873 62

The roles of sialyl-Lewisx antigen were evaluated in the pathogenesis of psoriasis. Sialyl-Lewisx expression was investigated immunohistochemically in the epidermis of normal human skin and erythematous lesional skin of psoriasis vulgaris by avidin-biotin-peroxidase complex procedures. A few sialyl-Lewisx positive dendritic cells were detected in the epidermis of normal human skin. In 7 out of 9 cases of psoriasis vulgaris, the number of sialyl-Lewisx-positive epidermal dendritic cells increased in the erythematous lesion over the adjacent normal skin; there were no marked changes in the numbers of CD1a-positive cells in the epidermis between the two skin types. In the double immunofluorescence studies, more than half of the sialyl-Lewisx-positive epidermal cells in psoriatic erythema were stained with a monoclonal Lag antibody that specifically reacts with Birbeck granules and related structures of human Langerhans cells. Furthermore, we determined the changes in serum levels of sialyl-Lewisx antigens in patients with psoriasis. Although levels in the sera were not significantly elevated over those of controls, the increases correlated with the degree of disease activity. These findings suggest that sialyl-Lewisx antigen is possibly involved in the development of psoriasis.
J Dermatol 1996 Feb
PMID:Evaluation of sialyl Lewisx antigen in the skin and the sera of patients with psoriasis vulgaris. 883 35

Cutaneous lymphocyte-associated antigen (CLA) defined by monoclonal antibody (MoAb) HECA-452 has been shown to be preferentially expressed on cutaneous T cells. The CLA expression has been regarded as a homing molecule of T cells to the skin in various inflammatory cutaneous disorders. In this paper we investigated the significance of CLA expression on Langerhans cells (LC) and found that, in normal skin, some epidermal LC express CLA, and that most dermal CD1a positive cells express CLA. When normal skin was organ cultured, the percentage of CLA positive cells in LC and dermal CD1a positive cells decreased appreciably. In diseased skin, epidermal LC increased in number and most LC expressed CLA. Thus, this study suggests that the CLA expression on LC may play as a homing molecule of LC to the skin.
J Dermatol Sci 1996 Jan
PMID:Expression of cutaneous lymphocyte-associated antigen defined by monoclonal antibody HECA-452 on human Langerhans cells. 886 63

We report the case of a boy with low expression of HLA class I molecules on peripheral blood mononuclear cells, which is associated with immunodeficiency. The patient, who had a Marfan-like phenotype, had chronic deep skin ulcers and sinobronchiectasis. Immunohistologic examination of the ulcerated skin showed a dense perivascular infiltrate composed of normal mature lymphocytes and macrophages. All cells in the infiltrate showed an apparently normal expression of HLA class I molecules, but intraepidermal dendritic Langerhans' cells were negative for CD1a, an antigen that is a highly specific marker for these cells and is abundantly expressed in some self-healing forms of cutaneous lesions. It is therefore speculated that a defective expression of CD1a molecules can contribute to the chronic persistence of deep skin ulcers, which have already been reported in association with defective expression of HLA class I molecules.
J Am Acad Dermatol 1996 Nov
PMID:Defective expression of HLA class I and CD1a molecules in boy with Marfan-like phenotype and deep skin ulcers. 891 93

Langerhans cells appear to be critical for IgE-mediated allergen capture and presentation in human atopic dermatitis. The present study sought to determine whether epidermal (i.e Langerhans cells) and dermal dendritic cells in the skin of dogs with atopic dermatitis are hyperplastic and expressed surface IgE. Frozen sections of lesional or non-lesional atopic and normal control canine skin were immunostained with CD1a-, CD1c-, and IgE-specific monoclonal antibodies. The enumeration of cells was performed by morphometry in both the epidermis and the dermis. Cell counts were compared with each individual's total serum IgE levels. Higher numbers of epidermal and dermal dendritic cells were present in atopic dogs than in normal control animals. Epidermal Langerhans cell counts were significantly higher in lesional than in non-lesional atopic specimens. IgE+ dendritic cells were observed in lesional atopic epidermis and dermis, and non-lesional atopic dermis, but not in normal control skin specimens. The percentages of IgE+ dendritic cells were correlated with each patient's total serum IgE levels. These results demonstrate dendritic cell hyperplasia and IgE expression in canine atopic dermatitis. Increased epidermal Langerhans cell counts in lesional specimens suggest an epidermal allergen contact in canine atopic dermatitis.
Arch Dermatol Res 1996 Sep
PMID:Langerhans cell hyperplasia and IgE expression in canine atopic dermatitis. 891 40

Recent reports point to a role for interleukin-12 (IL-12) in regulating T- and NK-cell function, macrophage activation and initiation of Th1-type cell responses. We sought to determine whether CD1a+ dendritic cells of the skin, as major antigen-presenting cells, are a source of IL-12 and therefore important in the initiation of Th1-type cell responses. To investigate this hypothesis, we cannulated microsurgically a skin-draining lymph vessel in the lower legs of five healthy volunteers. Altogether, ten different samples, each consisting of 1 x 10(6) lymph cells, were investigated. In four of the ten samples. CD1a+ dendritic lymph cells were isolated and purified by positive selection using mouse anti-CD1a monoclonal antibodies and sheep anti-mouse antibody-coated Dynabeads. Messenger RNA levels were estimated using a nested reverse transcriptase polymerase chain reaction (nRT-PCR) method. Total RNA was extracted from the cells, reverse transcribed to cDNA and amplified using specific primers for the target gene. Amplified products were sized by electrophoresis and visualized by ethidium bromide. Expression of IL-12 p40 and p35 mRNA was detected in all samples, both whole lymph samples and the highly enriched CD1a+ dendritic cell population. Our findings demonstrate that human skin-derived CD1a+ dendritic lymph cells produce IL-12 mRNA and may therefore be an important source of IL-12. Thus one might speculate that these CD1a+ dendritic cells, through their IL-12-producing capacity, might significantly influence the balance of Th1 versus Th2 reactions ultimately occurring.
Arch Dermatol Res 1996 Feb
PMID:IL-12 gene expression in human skin-derived CD1a+ dendritic lymph cells. 893 85

Immunological mechanisms play an important role in the pathogenesis of psoriasis. Lesional psoriatic skin-derived T-cell clones have been shown to stimulate keratinocyte proliferation and to predominantly express a T-helper type 1 cytokine pattern. However, T-helper type 2-like cytokines have also been identified in some psoriatic T-cell clones. In parallel to the T-helper type 1/type 2 dichotomy, a distinction between interferon-gamma-induced (classically activated) macrophages and interleukin-4/glucocorticoid-induced (alternatively activated) macrophages has been put forward as a conceptual framework for a better understanding of immunopathological processes. In the present study, the phenotype of mononuclear phagocytes in psoriatic skin lesions (n = 21), allergic contact dermatitis (n = 4) and normal skin (n = 2) was investigated using a panel of monoclonal antibodies (mAb) against monocytes/macrophages and dendritic cells (mAb MS-1, RM 3/1, and 25F9 against subsets of in vitro alternatively activated macrophages, and mAb against myeloid antigens CD1a, CD11b, CD11c, CD34, CD36, and CD68). With regard to mononuclear phagocytes, psoriatic skin was found to be compartmentalized into epidermis, subepidermal space, and upper and lower dermis. RM 3/1++ +, MS-1+/-, 25F9- dendritic macrophages previously classified as type II alternatively activated macrophages were the dominant dermal macrophage population in psoriatic skin, while intraepidermal and epithelium-lining macrophages expressed a different, presumably classically activated, macrophage phenotype (RM 3/1-, MS-1-, 25F9-, CD68+2, CD11b+2). In allergic contact dermatitis, a classical T-helper type 1 disease, RM 3/1++ + macrophages were less prominent. Since MS-1 high molecular weight protein is much more sensitive to interferon-gamma-induced suppression than RM 3/1 antigen, a predominance of T-helper type 1 cytokines in psoriasis could explain why dermal dendritic macrophages do not express the fully induced MS-1++ +, RM 3/1++ +, 25F9+/- phenotype of type I alternatively activated macrophages.
Arch Dermatol Res 1996 Nov
PMID:Immunohistochemical identification of type II alternatively activated dendritic macrophages (RM 3/1+3, MS-1+/-, 25F9-) in psoriatic dermis. 895 Apr 56

We postulate that wound healing is an orderly process mediated by a programmed expression of cytokines and growth factors. We suggest that these factors are produced in a consistent sequence, in regulated quantities and eliminated when their function is complete. We report here the results of studies on several cytokines, growth factors and the intercellular adhesion molecule expressed during the healing of grafts were visible clinically around 3-5 days post-graft and were completed by 4 weeks post-graft. During the 1st 2 weeks, we observed the following. (i) K-14 keratin was prominent throughout the entire epidermis. Thereafter it was limited to basal cell layers. (ii) Langerhans cells were not detectable with anti-human CD1a antibodies during the first week of healing but were clearly detectable 2 weeks post-graft. (iii) DOPA (dihydroxy phenylalanine) positive melanocytes gradually increased with time. The epidermis 21 to 28 days post-graft clinically and histologically seemed to be morphologically intact. Interleukin-1 (IL-1) was clearly detected in some basal cells of the epidermis, especially in melanocytes and some keratinocytes during the early stage of healing. Transforming growth factor-alpha (TGF-alpha) was detected in epidermis first in melanocytes and some keratinocytes shortly after grafting and again in the late stage of healing. It was also found in some dermal cells. Its expression coincided with keratinocyte proliferation and melanocyte migration. TGF-beta was strongly expressed in the epidermis and dermis after the first week post graft. (iv) ICAM-1 was transiently expressed only at the onset of healing. We previously reported that pro-opiomelanocortin and its derivatives MSH/ ACTH are expressed strongly during the healing of human xenografts. The 4 additional molecules which are the subject of this report all are expressed in healing human skin in a predictable sequence and quantity (intensity of stain). Together these data support our hypothesis that healing is a highly regulated process mediated by numerous cytokines.
Exp Dermatol 1997 Feb
PMID:The expression of cytokines, growth factors and ICAM-1 in the healing of human cutaneous xenografts on nude mice. 906 2

Opioid peptides are synthesized in neurons, endocrine cells, monocytes/macrophages and B and T lymphocytes. They interact with opioid receptors located on immune cells and nociceptive nerve terminals. Because opioid peptides might be of importance in inflammatory skin diseases, for example psoriasis, sections of skin from psoriatic patients were immunohistochemically stained with antisera against methionine and leucine enkephalin, CD68 (KP1, PG-M1), calprotectin (M747), M130 (Ber-MAC3), CD1a and CD3. Enkephalin-like activity was detected selectively in dermal CD68-positive macrophages/monocytes. The activity showed no association with the activation markers M747 and Ber-MAC3. There was a statistically significant increase in enkephalin-positive cells in involved psoriatic skin compared with uninvolved and normal skin. These results were confirmed by radioimmunoassay which showed elevated levels in extracts from involved psoriatic skin compared with uninvolved skin (81%) and normal skin (204%). Furthermore, preproenkephalin mRNA of an expected size was detected in involved psoriatic skin. If the increased levels of enkephalins present in monocytes/macrophages in psoriatic skin lesions reach the threshold for biological activity, they may play a role in the regulation of the inflammatory processes seen in this skin disease.
Arch Dermatol Res 1997 Apr
PMID:Enkephalin-like immunoreactivity in human skin is found selectively in a fraction of CD68-positive dermal cells: increase in enkephalin-positive cells in lesional psoriasis. 916 36

Protein kinase C (PKC) isoenzymes transduce signals from cell surface receptors and thereby regulate important cellular functions in skin including keratinocyte growth and differentiation. Overexpression of individual PKC isoenzymes results in aberrant cell growth and in certain instances tumorigenicity. PKC is implicated in tumour promotion in mouse skin. Abnormal expression of PKC has been reported in several human cancers. We have, therefore, investigated expression of PKC-alpha and -beta in basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) by immunohistochemistry. Sections were stained with specific antibodies to PKC-alpha, PKC-beta, CD1a, T cells, B cells and dermal dendritic cells (factor XIIIa), using an immunoperoxidase technique. PKC-alpha and PKC-beta were not detected in tumour cells in BCCs or SCCs. In SCCs, PKC-beta immunostaining revealed positively stained inflammatory and dendritic cells scattered through the stroma; PKC-alpha immunostaining was essentially negative. In contrast, in BCCs, PKC-alpha+ and PKC-beta+ dendritic and spindle-shaped cells were observed in the stroma, immediately adjacent to the tumour islands. Double-labelling experiments showed that a proportion (approximately 20%) of PKC-beta+ dendritic cells also expressed factor XIIIa. BCCs depend on stroma for growth; PKC regulates expression of type IV collagenase and stromelysin III and interactions between tumour and stroma may be important in determining tumour invasion and metastasis. Therefore, overexpression of PKC-alpha and -beta by stromal dendritic cells in BCCs suggests that PKC activation may be involved in stromal/tumour interactions in these tumours.
Br J Dermatol 1997 May
PMID:Overexpression of protein kinase C-alpha and -beta isozymes by stromal dendritic cells in basal and squamous cell carcinoma. 920 96


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