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, 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.
J Invest Dermatol 1980 Jul
PMID:Expression of Ia antigens on Langerhans cells in mice, guinea pigs, and man. 644 83

Epidermal Langerhans cells exhibit many features of macrophages/monocytes. Both bear surface receptors for the Fc portion of immunoglobulin molecules and the C3b complement component. Both take up, process, and present antigens to reactive lymphocytes in an effective fashion, and they display on their cell surfaces the alloantigenic determinants encoded by the I region of the major histocompatibility complex. In view of these facts, we explored the extent to which cutaneous sites with unusual immunologic attributes might correspondingly have maldistributions or decreased surface densities of Langerhans cells. Common body sites such as the ear, back, and abdominal wall skin in hamsters, mice, and guinea pigs had regularly distributed ATPase-positive Langerhans cells in surface densities between 500 and 1,500 cells/mm2. In contrast, hamster cheek pouch epithelium had fewer than 200 Langerhans cells/mm2 and murine tail skin exhibited both a decreased density and an unusual gridlike distribution of the cells. Langerhans cells were never demonstrated in corneal epithelium. Perturbation of body wall skin with ultraviolet light and with dinitrofluorobenzene temporarily depleted the skin of ATPase-positive Langerhans cells. Heterotopic grafts of hamster cheek pouch and murine tail skin tended to accumulate Langerhans cells and to become more like body wall skin. The concordance of Langerhans cell aberrations and unusual immunologic features of corneal cheek pouches and tail skins suggests the possibility that intentional perturbations of surface Langerhans cells, as with UVL, might achieve unusual immunologic reactions within normal body wall skin.
J Invest Dermatol 1980 Jul
PMID:Natural and perturbed distributions of Langerhans cells: responses to ultraviolet light, heterotopic skin grafting, and dinitrofluorobenzene sensitization. 644 86

The distribution of ATPase-positive Langerhans' cells was investigated in whole sheets of the glabrous sole-of-foot epidermis of the mouse. This completely orthokeratinizing tissue shows distinct morphological differences mainly with regard to the dermo-epidermal junction. Whereas the sharply outlined nodular prominences in the center of each footpad have a heavily undulated dermo-epidermal junction, the epidermal baseline in the surrounding tissue and the region just proximal to the footpad is flat. A dense population of evenly distributed ATPase-positive Langerhans' cells is found in the epidermis which surrounds the nodular structures. A slightly reduced population of Langerhans' cells is located in the epidermis of 80% of the nodules, occasionally showing a concentration in the pronounced epidermal ridges. Twenty percent of the nodules possess an epidermis which is completely free of Langerhans' cells. The results are discussed in view of the current hypothesis on the biological function of Langerhans' cells.
Arch Dermatol Res 1980
PMID:Langerhans' cell-free regions in orthokeratinizing sole-of-foot epidermis of the adult mouse. 644 86

This report defines the influence of ultraviolet light (UV) on Langerhans cells (LC). Human volunteers and hairless mice (Swiss ha/ha) were exposed to various single and/or cumulative doses of either UV-A, UV-B, or UV-A plus small amounts of UV-B (UV-A (+B)). 24 hr after the last irradiation, morphology of the entire epidermis was evaluated by both light and electron microscopy while LC, in addition, were tested for expression of specific histochemical (ATPase) and functional immunological markers (Ia antigens). In both men and mice, cumulative doses of either 80-120 J/cm2 UV-A (+B) or 1-2 X 100 J/cm2 UV-A resulted in a dramatic reduction of cells exhibiting ATPase and Ia-reactivity. In the UV-B spectrum, single doses of 60-80 mJ/cm2 produced a virtually complete elimination of LC membrane markers. By contrast, pemphigus antigens of keratinocytes were unaffected by these energy doses. Electron microscopy revealed cellular damage of some LC after UV-doses which produce a virtually complete abolition of LC membrane markers. At certain dose ranges (15-30 mJ/cm2 UV-B and 1 x 40 to 2 x 100 J/cm2 UV-A) LC were the only epidermal cells to display morphological damage at the ultrastructural level whereas higher doses affected all epidermal cells. The finding that LC surface markers and to a lesser extent the cells themselves are particularly susceptible to UV irradiation has important implications in view of previous findings that LC are potent stimulators of antigen-specific and allogeneic T cell activation. UV-induced alteration of LC plasma membrane integrity may represent a tool to manipulate adverse immune reactions involving the epidermis.
J Invest Dermatol 1981 Mar
PMID:Ultraviolet light depletes surface markers of Langerhans cells. 645 5

The effect of 8-methoxypsoralen plus long-wave ultraviolet light (PUVA) on Langerhans cell was examined in guinea pigs using ATPase staining method. The number of ATPase-positive Langerhans cells gradually decreased until 5 to 7 days after PUVA treatment, when it was found to be less than 10% to 20% of the original density. Even the ATPase-positive cells exhibited abnormal appearance. The dendritic processes were shortened or disappeared and the central body became oval or round. These changes in population and morphology of Langerhans cell almost returned to normal by 14 days. The inhibitory effect of PUVA on the induction of contact hypersensitivity may be partly due to the alterations of Langerhans cells. Furthermore, the damage on the antigen-presenting cells may accelerate the development of PUVA-induced tumors.
J Invest Dermatol 1981 Oct
PMID:The effect of 8-methoxypsoralen and long-wave ultraviolet light on Langerhans cell. 645 13

Sheets or sections of mouse epidermis reacted by a histochemical method for the enzyme beta-glucuronidase display a subpopulation of dendritic cells which correspond in number and spacing to Langerhans cells demonstrated by reactivity for ATPase or Ia antigens. A similar staining pattern is seen in rat, rabbit, and guinea pig epidermis. In rhesus monkey and human skin, Langerhans cells appear to be reactive for beta-glucuronidase but, as keratinocytes are also reactive, Langerhans cells are not readily identifiable by this method. The thermal stability of beta-glucuronidase differs between strains of mice. Langerhans cells of Balb/C and C3H strains can thus be distinguished by appropriate pretreatment before incubation, a method of potential value for experimental investigations of the origin of Langerhans cells.
J Invest Dermatol 1982 Mar
PMID:Reactivity of epidermal Langerhans cells to a histochemical method for demonstration of beta-glucuronidase. 646 65

Five patients with autosomal dominant ichthyosis vulgaris (ADI) were studied to see whether the abnormal keratinization was associated with disturbances of the appearance or the distribution of epidermal Langerhans cells (LCs). The LCs were identified by ATPase staining and electron microscopy. They were present in normal numbers, were of normal morphology and were in their usual mid-epidermal position. These observations do not support the hypothesis that LCs are involved directly in the process of keratinization.
Br J Dermatol 1983 Sep
PMID:Langerhans cells in autosomal dominant ichthyosis vulgaris. 661 17

Epidermal Langerhans cells resemble macrophages/monocytes in several remarkable ways: both bear surface receptors for the Fc portion of immunoglobulin molecules and for the C3b complement component. They take up, process and present antigen to reactive lymphocytes in an extremely effective fashion. They display on their cell surfaces the alloantigenic determinants encoded by genes of the I region of the major histocompatibility complex. Using ATPase activity, Langerhans cell surface densities are abnormal in 3 cutaneous sites which exhibit unique immunologic properties: markedly reduced numbers in hamster cheek pouch; reduced numbers and uneven distributions in murine tail skin; no Langerhans cells occur within corneal epithelium. As a functional expression of the absence of Langerhans cells from murine corneas, allografts prepared from corneal epithelium fail to sensitize recipients to Ia antigens encoded by I region genes of the donor. Corneal grafts disparate from their hosts at only I region loci are accepted for at least 45 days. The absence of Langerhans cells from cornea may account in part for its property as an immunologically privileged tissue. Subthreshold numbers of Langerhans cells in cheek pouch epithelium may contribute significantly to the observations that the hamster cheek pouch is an immunologically privileged site. We infer that skin deficient in Langerhans cells may be consequently deficient in alloantigenicity. Equally important, Langerhans cell-poor skin may be lacking in certain essential functions relating to the induction and expression of immune reactivity.
J Invest Dermatol 1980 May
PMID:Unusual numbers and distribution of Langerhans cells in skin with unique immunologic properties. 699 73

The role of Langerhans cells in the induction of contact photosensitivity (CPS) to tetrachlorosalicylanilide (TCSA) was investigated in mice. CPS was induced by 2 daily paintings of 50 microliters of 1% TCSA in acetone plus black light irradiations for 2.5 hr. Both ears were challenged with 20 microliters of 0.1% TCSA in ethanol plus black light irradiation for 2.5 hr on day 5, and ear thickness was read at 24 hr. The density of LCs detected as ATPase-positive cells dramatically decreased 2 days after exposure to UVB. CPS was not induced by painting the photoallergen to the skin which had been pre-irradiated with UVB. The ear swelling response returned to the normal level when the mice were sensitized 12 days after UVB exposure in accordance with the complete regeneration of ATPase-positive cells. Dose of UVB in the present study did not affect the development of CPS through systemic mechanism. These demonstrations indicate that LCs play an important role in the induction of CPS.
J Invest Dermatol 1982 May
PMID:Mechanisms of contact photosensitivity in mice: II. Langerhans cells are required for successful induction of contact photosensitivity to TCSA. 706 12

An enzyme histochemical and cytochemical study of normal dermal microvasculature showed that respiratory enzymes, lipase and non-specific esterase occurred in all vascular segments. Lysosomal enzymes were also widely distributed and acid phosphatase activity was localized in lysosomes, Golgi apparatus and small portions of endoplasmic reticulum of both endothelial cells and pericytes. Alkaline phosphatase activity, however, was confined to the arterial side and tip of the capillary loop where it occurred in vesicles along the luminal surface of the endothelium and in junctions between endothelial cells. The localization of nucleoside phosphatase activity within the endothelium varied according to substrate; with adenosine triphosphate as substrate, the reaction product occurred in vesicles distributed throughout the endothelial cells; with adenosine diphosphate it was limited to vesicles along the luminal surface; and with adenosine monophosphate, activity was mostly localized to the lateral surfaces of endothelial cells. These findings suggest functional variation between different vascular segments and between various components of the endothelium. Attempts to demonstrate a specific Na+K+ adenosine triphosphatase (transport ATPase) within the endothelium were not successful.
Br J Dermatol 1981 May
PMID:Human dermal microvasculature: II. Enzyme histochemical and cytochemical study. 723 11


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