Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In all mammalian species so far examined, Langerhans cells or their precursors are the only epidermal cells expressing Ia antigens or their equivalents. In man, xeno-antisera raised in rabbits against purified B-lymphocyte cell membrane antigens were utilized to stain the Langerhans cells by either fluorescent or immunoferritin methods. As high proportion of the indeterminate cells in the epidermis also expressed HLA-DR antigens, and a relationship to Langerhans cells is suggested. Confirmation of these results was obtained in mouse. Alloantisera raised against I-A and I-EC subregion products again stained only Langerhans cells. Fluorescent, immunoperoxidase, and immunoferritin methods were used and confirmation of the specificity of the reaction was achieved at the electron microscope level. Langerhans cells were shown by ATPase staining to be absent from the epithelium of the central cornea, but present in the limbus. Population of the entire corneal epithelium surface was induced by application of irritants or contact sensitizing agents such as DNCB. Grafting of corneas either deficient or populated with Langerhans cells, to skin beds, may answer the question of the influence of such cells on allograft rejection.
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PMID:The Langerhans cell. 617 52

A combination of immunochemical staining for HLA-DR antigens and the histochemical demonstration of enzyme activity has been used to identify specific cell populations in the normal and arthritic synovial lining layers. Such combined staining has revealed that the normal synovial lining contains a proportion of HLA-DR + ve cells, all of which show strong lysosomal enzyme activity. This population is greatly expanded in biopsies from patients with osteoarthritis and these positive cells also express strong ATPase activity. In the rheumatoid synovium five distinct cell types can be identified; all of which are HLA-DR + ve but differ in their morphology and pattern of enzyme activity. Of special interest was the discovery that a small but significant proportion of these cells have the characteristics of the interdigitating cells of the lymph node paracortex. The relationship between the emergence of these heterogeneous populations and the immunological basis of this inflammatory response is discussed.
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PMID:Histochemical discrimination of HLA-DR positive cell populations in the normal and arthritic synovial lining. 621 28

Epidermal Langerhans cells (LCs) possess surface markers and functional attributes which identify them as being of macrophage/monocyte lineage, and recent evidence documents their participation in certain immune process which occur in skin. To assess the role of LCs in lupus erythematosus (LE), a disease in which immune system dysfunction predominates, human epidermis from patients with cutaneous LE was studied with 3 LC surface markers: ATPase activity, HLA-DR and OKT-6 antigens. Suction blister top epidermal skin biopsies from patients with 3 clinical types of cutaneous LE exhibited similar features: LCs were less dendritic, they were more irregularly distributed, and they were present in fewer numbers when compared with those in adjacent normal skin. These changes contrasted with those observed in diseases with similar lichenoid histopathological features. LCs appeared increased in number in lichen planus. LCs in skin lesions from one patient with dermatomyositis exhibited similar morphologic alterations, but surface densities and distributions were preserved. Disaggregated epidermal cells from skin lesions of patients with cutaneous LE induced allogeneic lymphocyte proliferation as efficiently as did cells from nonlesional skin, indicating that the morphologic alterations observed were not associated with a decreased alloantigen presenting capacity. These studies have demonstrated that epidermal LC populations in 3 clinical types of cutaneous LE are perturbed in a manner not seen in 2 other lichenoid skin diseases, although these changes were not associated with an altered capacity of such cells to stimulate proliferation by allogeneic lymphocytes.
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PMID:Epidermal Langerhans cell involvement in cutaneous lupus erythematosus. 621 51

Epidermal Langerhans cells (LCs) function as the antigen-presenting cells in such cutaneous cell-mediated immune responses as contact hypersensitivity and in the mixed epidermal cell-lymphocyte reaction. They have also been implicated in the immune response in skin allograft rejection. Since organ culture of thyroid and pancreas has been shown to prolong allograft survival, presumably through the loss of antigen-presenting cells, we examined the effect of skin explant culture on LC survival. Human skin explants were placed in organ culture and examined serially as whole mounts of epidermis for the presence of LCs as judged by ATPase activity, and OKT-6 and HLA-DR antigens. Although we observed morphologic changes and an absolute reduction in the number of positively stained cells, culture for up to 28 days failed to deplete explants of these cells. Langerhans cells were also sought in the epidermal outgrowths that develop peripheral to the original explants. They were never seen in the area beyond 0.3 mm from the explant edge. Organ culture of skin thus provides a means to explore the contribution of LCs to skin allograft rejection by comparing the immunogenicity of epidermal portions of the explant with the epidermal outgrowth.
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PMID:Differential distribution of Langerhans cells in organ culture of human skin. 621 52

Macrophage like cells expressing high concentrations of HLA-DR antigen have been identified in situ within the synovium of patients with rheumatoid arthritis. The characteristics of these cells have been determined using immunohistological analysis and combined cytochemical techniques. It was found that the majority (greater than 80%) of these cells were interspersed within the perivascular lymphocytic infiltrates occurring in the synovium. These cells did not stain with antisera against surface immunoglobulin or any Mc Abs to T lymphocyte markers. Further combined staining demonstrated that the HLA-DR + ve cells did stain with an anti-monocyte monoclonal (FMC-17), but could not be stained with a Mc Ab against C3b receptors. The interfacing of cytochemical reactions for acid phosphatase (ACP) and adenosine triphosphatase (ATPase) with immunofluorescence staining for HLA-DR demonstrated that these cells were ACP - ve ATPase + ve. This analysis led to the conclusion that the HLA-DR + ve cells found in abundance in the rheumatoid synovium expressed identical characteristics to the interdigitating cells of the normal lymph node paracortex. The possible significance of the presence of large numbers of such antigen presenting cells in the rheumatoid synovium is discussed.
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PMID:The involvement of interdigitating (antigen-presenting) cells in the pathogenesis of rheumatoid arthritis. 622 Aug 47

Unlike keratinocytes, Langerhans cells express both surface ATPase activity and Ia (HLA-DR) antigens. A well-characterized in vitro system containing Langerhans cells would be of great use in elucidating their functions. Thus, epidermal cell cultures derived from neonatal Balb/c mice were examined for the presence of Langerhans cells. Twenty-four hours after initiation of culture, ATPase- and Ia-positive cells were seen to be associated with cell aggregates. By day 3, Langerhans cells migrated on to the substratum and, as the cultures matured and stratified, were seen both in groups and as single cells for the duration of the cultures (day 14). During culture, although the total number of cells increased, the percentage of cells expressing Ia antigen and ATPase activity remained constant, suggesting that Langerhans cells increase in number during cell culture. Such a situation could arise from actual division of Langerhans cells during culture or from latent expression of Ia antigen and ATPase activity by pre-existing cells. This is the first study of the dynamics of Langerhans cells in a cell culture system and shows that Langerhans cells are present throughout the lifespan of the cultures.
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PMID:Dynamics of Langerhans cells in genetically defined murine epidermal cell culture. 623 98

HLA-DR-positive histiocytes in the lamina propria of the human intestine have been characterised using combined histochemical and immunohistological techniques. In the small intestine, 80-90% of the HLA-DR+ histiocytes had irregular surfaces with stellate processes, and exhibited strong membrane adenosine triphosphatase (ATPase) activity, but weak acid phosphatase (ACP) and non-specific esterase (NSE) activities (HLA-DR+ ACP+/- NSA+/- ATP++; type 1 cell). In contrast, in the lamina propria of the colon the majority (60-70%) of HLA-DR+ cells were large, round cells with strong ACP and NSE activities but no detectable ATPase activity (HLA-DR+ ACP++ NSE++ ATP+/-; type 2 cell). The colon also contained a population of type 1 cells (30-40%). In active inflammatory bowel disease affecting the colon a third population of HLA-DR+ histiocytes was seen. These cells were irregular in outline, with many processes, and were ACP++ NSE+ ATP+/- (type 3 cell). The type 3 cells appeared to replace type 2 cells. After treatment, the appearances returned to normal. These findings suggest that the different populations of HLA-DR+ histiocytes in the human intestine may have several functions, reflecting the different forms of antigen present in the intestine. The alterations in inflammatory bowel disease may represent activation in response to an invading antigen.
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PMID:Heterogeneity of HLA-DR-positive histiocytes in human intestinal lamina propria: a combined histochemical and immunohistological analysis. 633 64

In vivo studies have demonstrated that various treatments of skin, e.g., UV irradiation, topical corticosteroids, and tape-stripping, will temporarily deplete the epidermis of Langerhans cells (LC). Whether this loss represents simply a loss of cell surface markers unique to LC, or actual depletion of cells, is unknown. By design, normal human skin transplanted to the congenitally athymic (nude) mouse is a system devoid of circulating precursors for human LC. Because LC have been shown to be of bone marrow origin, any depletion of these cells in this system should be permanent. Treatments to deplete LC from human skin grafts on nude mice after grafting included: (a) large doses of UV radiation (400 mJ/cm2 every 48 h, X 3), (b) potent high-dose topical corticosteroids (2.5 mg betamethasone valerate/cm2 every day, X 5), (c) tape-stripping (X 20). Treatments before grafting included: (a) treating donor skin with 900 R of gamma irradiation, (b) complement fixing monoclonal antibody to Ia-like antigens of LC, followed by fresh complement, (c) monoclonal antibody conjugated to toxins. Quantitation of the number of LC was analyzed on control and treated epidermal sheets using immunodiagnostic reagents, anti-HLA-DR, and surface ectoenzymes , ATPase. Results show that both UV irradiation and topical corticosteroids reduce the number of LC by these analyses. However, within 3 weeks, recovery to pretreatment levels has occurred. X-irradiation and tape-stripping were without effect. Despite evidence that the monoclonal antibody, complement, and toxic systems were delivered to the LC within the epidermis, there is no evidence that these treatments resulted in a decrease in LC. It appears that LC are currently either long-lived or replaced locally from a proliferative pool and that certain cell membrane determinants of human LC are somewhat differentially sensitive to UV radiation and corticosteroids.
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PMID:Biology of Langerhans cells: analysis by experiments to deplete Langerhans cells from human skin. 637 58

In all mammalian species so far examined, Langerhans cells or their precursors are the only epidermal cells expressing Ia antigens or their equivalents. In man, xenoantisera raised in rabbits against purified B lymphocyte cell membrane antigens were utilized to stain the Langerhans cells, by either fluorescence or immunoferritin methods. A high proportion of the indeterminate cells in the epidermis also expressed HLA-DR antigens, and a relationship to Langerhans cells is suggested. Confirmation of these results was obtained in mouse. Alloantisera raised against I-A and I-EC subregion products again stained only Langerhans cells. Fluorescence, immunoperoxidase, and immunoferritin methods were used, and confirmation of the specificity of the reaction was achieved at the electron microscope level. Langerhans cells were shown, by ATPase staining, to be absent from the epithelium of the central cornea, but were present in the limbus. Population of the entire corneal epithelium surface was induced by application or irritants or contact sensitizing agents such as dinitrochlorobenzene. Grafting of corneas either deficient or populated with Langerhans cells, to skin beds, may answer the question of the influence of such cells on allograft rejection.
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PMID:Expression of Ia antigens on Langerhans cells in mice, guinea pigs, and man. 644 83

FMC-17a monoclonal antibody reactive with peripheral blood monocytes was used to identify cells of monocyte origin in sections of normal and inflamed human tissues. FMC-17 + ve cells were found in all samples tested. The distribution, HLA-DR staining characteristics, and enzyme profiles (ACP and ATPase) of FMC-17 + ve cells indicated that interdigitating (dendritic) cells, Langerhans cells, tissue histiocytes, and the classical inflammatory phagocytic macrophages belonged to the reactive population. The antigen recognized by this antibody was found on monocytic and promonocytic cells in bone marrow, yet appeared to be lost following activation in the later stages of inflammatory conditions. Further studies are necessary to elucidate at what stage in the differentiation/maturation pathway the antigen is acquired and again whether or not FMC-17--ve cells are an activated or degenerating population.
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PMID:The reactivity of a monoclonal antibody against cells of the monocyte-macrophage series in sections of normal and inflamed human tissues. 665 44


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