Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study introduces a simple, reproducible assay for HLA class I antigen using antibodies against beta 2-microglobulin and the heavy chain on HLA. The sandwich technique was named mixed enzyme-linked immunosorbent assay (MELISA), and was designed for identification of plasma membranes in neutrophil subcellular fractions. The subcellular localization of HLA was identical to that of other plasma membrane markers, [3H]concanavalin A and detergent-independent alkaline phosphatase, and was unchanged by stimulation of cells by weak and strong secretagogues. In addition to the presence as part of the HLA complex in the plasma membrane uncomplexed beta 2-microglobulin is present in the specific granules of neutrophils. However, the release of beta 2-microglobulin from intact neutrophils stimulated with formyl-methionylleucylphenylalanine was much higher than could be explained by exocytosis of specific granules. Subcellular fractionation studies demonstrated that beta 2-microglobulin is localized in fractions characterized by latent alkaline phosphatase and released from this novel secretory compartment in response to stimulation with formyl-methionylleucylphenylalanine.
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PMID:Mixed enzyme-linked immunosorbent assay (MELISA) for HLA class I antigen: a plasma membrane marker. 218 25

We describe a mother and 2 daughters with familial recurrent calcific periarthritis in a family with an inherited tendency to develop generalized osteoarthritis (OA). Low levels of serum alkaline phosphatase were found in 1 of the daughters while the mother developed erosive OA in later life. HLA typing was noncontributory. However, the 3 individuals with periarthritis possessed blood group A+, while the 6 unaffected family members were O+. The experience of this family adds weight to the case that recurrent calcific periarthritis may be due to an inherited abnormality of alkaline phosphatase production and suggest that this may also be responsible for the recently observed association of calcific periarthritis and erosive OA.
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PMID:Recurrent calcific periarthritis, erosive osteoarthritis and hypophosphatasia: a family study. 192 Mar 24

We have studied the effect of maturation to small intestinal-like epithelial cells of the human colonic carcinoma cell line HT29 on the lateral mobility of different representative membrane components (lipid, proteins), as assessed with fluorescence recovery after photobleaching (FRAP). Maturation was induced in vitro in the HT29 cells by replacing glucose (Glu) with galactose (Gal) in the growth medium (DMEM) during a 21-day period. Scanning electron microscopy revealed an increased number of microvilli in the apical cell membrane, and enzyme analyses (alkaline phosphatase, aminopeptidase) in combination with aqueous countercurrent distribution, indicated that maturation was induced with DMEM-Gal. In comparison to control cells grown in DMEM-Glu medium, the more small intestinal-like cells grown in DMEM-Gal displayed no alteration of the lateral mobility of either cholera toxin (B subunit)-labelled ganglioside GM1 (diffusion coefficient, D [x 10(8)] = 0.8-0.9 cm2s-1; mobile fraction, R = 50-60%) or antibody-stained Class 2 histocompatibility (HLA-DR) antigen (D [x 10(9)] = 2 cm2s-1; R = 60-70%). However, antibody-labelled beta 2-microglobulin of HLA Class 1 antigen displayed increased mobility in HT29-Gal cells; D was x 1.4 and R x 1.8 larger in the HT29-Gal cells. By contrast, the mobility of a neoplastic antigen was reduced; D and R were x0.60 and x0.69 of the values seen in HT29-Glu cells. It is thus concluded that DMEM-Gal-induced differentiation in confluent HT29 cells is accompanied by specific rather than general effects on the lateral mobility of different membrane components.
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PMID:Small intestinal differentiation in human colon carcinoma HT29 cells has distinct effects on the lateral diffusion of lipids (ganglioside GM1) and proteins (HLA class 1, HLA class 2, and neoplastic epithelial antigens) in the apical cell membrane. 233 58

The expression of HLA class I and II antigens was analysed in 30 primary gastric carcinomas, 27 autologous lymph node metastases and 25 autologous gastric mucosae. We used an immune alkaline phosphatase technique on cryostatic sections and mAbs directed against HLA class I monomorphic determinants, HLA-B locus-specific products and HLA-DR, -DP and -DQ molecules. In addition HLA class I genes were analysed in tumour tissue and compared by Southern blots with the RFLP from autologous mucosa using locus-specific HLA probes. Finally the infiltrating mononuclear cells were studied on gastric tumours and adjacent mucosa with mAbs defining CD4, CD8 and CD11b differentiation antigens. The results obtained showed that three out of 27 primary gastric carcinomas completely lack HLA-ABC antigens (10%). In addition, two primary tumours presented a variable expression. The remaining 22 tumours presented a homogeneous positive HLA class I expression. Interestingly, when the autologous mucosa was analysed, only 12 out 25 specimens were homogeneously stained with mAbs against HLA class I antigens, suggesting that this tissue may lack the expression of HLA antigens before becoming malignant. Indeed, the majority of the gastric carcinomas studied presented a higher HLA-ABC antigenic expression than autologous mucosa. Finally, the HLA expression observed in the primary tumour was similar to that observed in autologous metastases. As a second part of the study we have found a direct relationship between the expression of HLA-DR antigens in mucosa and the intensity of inflammatory infiltration. This relationship was not maintained in the tumour tissue. In the mucosa the CD4-positive T cell was the predominant lymphocyte, while it was CD8 in the HLA-DR-positive tumours. Finally the RFLP of class I genes did not show any differences in any of the cases when compared with autologous mucosa. We included in these studies DNAs from HLA class I-negative tumours, HLA positive and HLA-B-negative ones.
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PMID:MHC class I and II antigens on gastric carcinomas and autologous mucosa. 263 12

Both cytoplasmic and surface-membrane antigens of human spermatozoa were detected by means of monoclonal antibodies (MoAbs) and of the alkaline phosphatase anti-alkaline phosphatase- (APAAP-) technique. Several advantages of this technique for the identification of sperm could be demonstrated. The labeling of cytocentrifuge preparations from 16 ejaculates proved the presence of glycosphingolipids, nuclear and mitochondrial antigens of spermatozoa. However, there were no HLA-molecules and other leukocyte antigens on sperm cells.
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PMID:Identification of human spermatozoa antigens using monoclonal antibodies and the alkaline phosphatase anti-alkaline phosphatase-technique. 265 9

A group of 170 patients having functional renal allografts were evaluated at least six months after renal transplantation. They were assessed for symptoms and signs of tendinitis in the Achilles and Supraspinatus tendons. Of the 170 patients, 34 had tendinitis. Four patients (11.8%) had spontaneous rupture of the Achilles tendon one week to 72 months after transplantation. All of the symptomatic patients had received steroids, and 81% of these had been treated with methylprednisolone. Of the asymptomatic patients 89% received steroid and 69% received methylprednisolone. There was a significant correlation between symptoms of tendinitis and the cumulative steroid dose. The number of matching HLA loci of the donor kidney and the length of time on dialysis were also related to the incidence of tendinitis. Unlike a previous study (1) we could not find significant differences between the 34 patients with tendinitis and controls with reference to the levels of serum phosphate, alkaline phosphatase, albumin adjusted calcium, or cholecalciferol therapy prior to transplantation. Our data confirm that tendinitis is surprisingly common in patients after renal transplantation (20.0%).
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PMID:Tendinitis--a common complication after renal transplantation. 279 10

To determine whether the mononuclear cells (MC) and multinucleated giant cells (GC) of giant cell tumor of tendon sheath (GCTTS) exhibit evidence of monocyte/macrophage lineage, we studied their antigenic features (seven cases, paraffin sections; two cases, frozen sections) and enzymatic features in situ (four cases, plastic sections). Both MC and GC expressed a monocyte/macrophage phenotype: HLA-A,B,C+, HLA-DR+, T200+ (leukocyte common antigen), Leu-M3+ and Leu-3+. MC and GC also expressed similar enzymatic phenotypes which resembled that of osteoclasts. Both were rich in acid phosphatase and contained smaller, variable amounts of ATPase, beta-glucuronidase, alpha-naphthyl acetate esterase, and 5'-nucleotidase. Both lacked alkaline phosphatase. Reactive osteoclasts in plastic and paraffin sections were also T200+, a finding strongly supporting their bone marrow derivation and leukocytic differentiation. In plastic sections, osteoclasts were additionally reactive with macrophage antigen EBM11. In aggregate, these data suggest that GCTTS is a true histiocytic lesion of monocyte/macrophage lineage composed of phenotypically similar MC and GC that most closely resemble osteoclasts. We found no evidence that GCTTS cells resemble osteoblasts, fibroblasts, or synovial sarcoma cells. Furthermore, expression of the Ki-67 nuclear antigen by 1-2% of MC but not by GC suggests that the proliferating cells in GCTTS are restricted to its MC component.
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PMID:The cells of giant cell tumor of tendon sheath resemble osteoclasts. 283 1

The relationship between T nodules and adjacent B-lymphoid follicles was investigated in 37 reactive lymph nodes by light microscopy and combined enzyme immunohistochemistry. In 16 cases (43%), T nodules and adjacent B-lymphoid follicles were unified in an ovoid, distinct nodular structure termed a "composite nodule." The composite nodule comprises two separate domains. The peripheral, subcapsular B domain contains all stationary and migratory elements of the B-lymphoid follicle, ie, B1+ B-cells, OKT4+, Leu 3a+ helper/inducer T cells, HLA-DR+ dendritic reticulum cells, and ANAE+, AcPhase+ tangible body macrophages and is surrounded by a B1+, HLA-DR+ lymphocytic corona displaying focal adenosine triphosphatase (ATPase) and alkaline phosphatase (AlkPhase) activity. The deep, paracortical T-domain contains all elements of the T nodule, ie, OKT4+, Leu3a+ helper/inducer T cells, high endothelial venules and HLA-DR+, ATPase+ interdigitating reticulum cells. The composite nodule is surrounded by a rim of ATPase+, AlkPhase+ high endothelial venules. Both domains are subject to changes in volume; thus, in follicular hyperplasia, the B domain enlarges at the cost of the T domain, and the reverse may occur in T-zone hyperplasia. Based on the striking resemblance between the composite nodule and the white pulp of the spleen, it is suggested that the composite nodule plays a major role in the triggering, helper-T-cell-dependent stimulation and subsequent maturation of antigen-responsive B cells into antibody-secreting plasma cells.
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PMID:The composite nodule. A structural and functional unit of the reactive human lymph node. 293 88

The unique curability of gestational trophoblastic tumors may in part be attributable to a host immunologic response. The occurrence of rapidly progressive and fatal choriocarcinoma may be favored by histocompatibility between patients and their partners. However, histocompatibility is not a prerequisite for the development and persistence of gestational choriocarcinoma. The expression of HLA by choriocarcinoma cells in culture is enhanced following incubation with gamma-interferon and this may be of both biologic and clinical significance. Complete molar pregnancy is a complete allograft because all molar chromosomes are of paternal origin. Patients with complete mole are sensitized to paternal HLA antigen which is expressed in molar tissue. Other polymorphic antigen systems including trophoblast-leukocyte common antigens and placental-type alkaline phosphatase are also expressed in molar tissue. We have studied the immunopathology of the molar implantation site to investigate possible humoral and cellular immune responses. The relationships among normal placenta, complete mole and choriocarcinoma are not clearly understood. The pattern of expression of oncofetal antigens in these three gestational tissues may be used to assess trophoblastic differentiation. In studies to date, molar trophoblast has the same pattern of expression of oncofetal antigens as normal placental trophoblast. We will review recent advances in our understanding of the immunobiology of gestational trophoblastic disease and suggest new directions for further research.
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PMID:Immunobiology of complete molar pregnancy and gestational trophoblastic tumor. 303 May 77

Histogenesis of cardiac myxoma is still unclear. Beside endothelial cells a variety of different cell types were detected in this benign cardiac tumor. Cryostat sections of four myxomas were analysed in the indirect immunoperoxidase technique using monoclonal antibodies (MoABs) directed against MHC class I and II antigens, as well as different surface determinants specific for endothelial cells or monocytes/macrophages. Tumor cells forming cell clusters and blood vessel like structures differed in their expression of endothelial antigens suggesting cellular heterogeneity within single and different myxomas. Like in fetal cardiac tissue vascular channels rarely carried HLA-class II antigens. Tumor cells carrying antigens of monocytes/macrophages, as well as intracellular alkaline phosphatase of endothelial cells could represent subpopulations of an early differentiation stage. This analysis further supports previous hypothesis of an endothelial origin of myxomas.
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PMID:[Phenotypic heterogeneity of cardiac myxomas]. 332 41


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