Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The formyl peptide receptor (FPR) and the glycosyl-phosphatidylinositol-linked type III receptor for the Fc portion of IgG (Fc gamma RIIIB; CD16) play important roles in various inflammatory responses in human neutrophils. The mechanisms of signaling by the glycosyl phosphatidylinositol-anchored Fc gamma RIIIB are not known. Therefore, we investigated the possibility that Fc gamma RIIIB and FPR may act in concert to mediate neutrophil functions. We observed that pretreatment of normal human neutrophils with Fab fragments of a mAb to the Fc gamma RIII (3G8) specifically inhibited their chemotaxis into micropore filters in response to the formylated peptides FMLP or formyl-norleucyl-leucyl-phenylalanine. Pretreatment of neutrophils with a saturating concentration of 3G8 Fab (100 nM or 5 micrograms/ml) followed by exposure to FMLP (0.5 to 500 nM) indicated that significant inhibition of chemotaxis was observed at peptide concentrations greater than 5 nM. However, 3G8 Fab had no effect on the neutrophil response to a wide range (0.05 to 500 nM) of other chemotactic factors, including C5a, leukotriene B4, IL-8 (neutrophil-activating peptide-1), and platelet-activating factor. Moreover, pretreatment of neutrophils with mAb to other cell surface molecules (decay-accelerating factor, Fc gamma RII, and HLA class I) did not affect chemotaxis to FMLP. Inhibition of movement was not due to degradation of FMLP by the cell surface endopeptidase 24.11 (CD10), because neutrophils pretreated with the CD10 inhibitor phosphoramidone and 3G8 Fab displayed the same altered response to FMLP as cells pretreated with 3G8 Fab alone. Ligation of the Fc binding site of Fc gamma RIIIB appears to be essential for altering the FMLP-induced response, since soluble aggregated IgG and other anti-Fc gamma RIII antibodies, all of which recognize the ligand binding site, mimic the inhibitory effect of the 3G8 Fab on FMLP-induced chemotaxis. In contrast, a mAb (214.1) that does not recognize the Fc binding site of Fc gamma RIIIB had no effect on FMLP-induced chemotaxis. Not only did anti-Fc gamma RIII inhibit neutrophil chemotaxis to FMLP in a filter-based migration assay, but 3G8 Fab also inhibited FMLP-induced neutrophil transendothelial migration. Scatchard plot analysis of radioligand binding experiments indicated that 3G8 Fab did not significantly alter the number of FMLP binding sites on neutrophils but significantly increased the affinity of the FPR for [3H]FMLP. Removal of greater than 80% of cell surface Fc gamma RIIIB by phospholipase C abolished the neutrophil chemotactic response to FMLP but did not affect movement toward C5a, IL-8, or leukotriene B4.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Human neutrophil Fc gamma RIIIB and formyl peptide receptors are functionally linked during formyl-methionyl-leucyl-phenylalanine-induced chemotaxis. 132 56

To provide baseline information on the immunoarchitecture of normal bone marrow, we studied cryostat-cut, frozen, and paraffin-embedded, fixed tissue sections prepared from 21 core biopsies of normal bone marrow obtained during bone marrow harvests for transplantation. A large panel of antibodies was applied that included, for frozen tissue, Leu-6 (CD1), T11 (CD2), Leu-3a (CD4), Leu-1 (CD5), Leu-2a (CD8), J5 (CD10), My7 (CD13), Leu-11 (CD16), B4 (CD19), B1 (CD20), B2 (CD21), Tac (CD25), My9 (CD33), T200 (CD45), NKH-1 (CD56), kappa and lambda chains, beta F1, Ki-67, HLA-DR, TQ1, and keratin, and for fixed tissue, leukocyte common antigen (CD45), L26 (CD20), LN1 (CDw75), LN2 (CD74), LN3, LN4, LN5, MB1 (CD45R), MB2, MT1 (CD43), MT2 (CD45R), UCHL1 (CD45R0), BM1, Ki-1 (CD30), Leu-M1 (CD15), lysozyme, KP1 (CD68), actin, S100, neuron-specific enolase, vimentin, and keratin. On fresh-frozen sections CD19 and CD2 were the most reliable and sensitive markers for B and T cells, staining 5% and 9% of marrow cells, respectively. Immunoglobulins generally showed heavy background staining, which frequently precluded an accurate assessment. The CD4 to CD8 ratio in the bone marrow was reversed from that of peripheral blood. On fixed tissues, leukocyte common antigen was found in 14% of the marrow cells, corresponding roughly to the lymphocyte population. L26, a pan-B-cell marker, stained 3% of the marrow cells. Among the other B-cell markers, LN1 and MB2 stained a large number of cells (40% to 70%), indicating reactivity with cells of the myeloid or erythroid series in addition to lymphocytes. Among the T-cell markers, UCHL1 and MT1 stained 66% and 50% of the cells, respectively, which could be explained by their cross-reactivity with myeloid cells. Nonspecific myelomonocytic markers (Leu-M1, KP1, and lysozyme) also showed reactivity in a high percentage of cells. No particular architectural distribution patterns of B or T lymphocytes were noted in either frozen or fixed bone marrow specimens. The results of this study provide normal baseline data for the immunohistologic application of hematopoietic and lymphoid markers on frozen or fixed bone marrow biopsy specimens.
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PMID:Immunoarchitecture of normal human bone marrow: a study of frozen and fixed tissue sections. 159 93

Rapid increases in the membrane expression of C3 receptors on granulocytes and monocytes in response to the anaphylatoxin C5a have previously been described. In this study we demonstrate increases in the membrane expression of neutral endopeptidase (NEP, CD10, CALLA), aminopeptidase N (APN, CD13), tyrosine phosphatase (CD45/CD45Ro) and the Fc R Fc gamma-RIII (CD16) on granulocytes within minutes of treatment with human C5a. Monocytes responded to C5a with increases in CD13 and CD45/CD45Ro. These membrane modulations could be prevented by preincubating the C5a preparations with anti-C5a mAb C17/5 but not by pretreating the cells with cycloheximide. Increases of CD10, CD13, and CD11b but not CD11a (LFA-1) were also observed in leukocytes from patients undergoing hemodialysis with cuprophan membranes. The increase of CD16 on granulocytes was dependent on the presence of plasma during in vitro activation with C5a indicating that plasma contains inhibitors which prevent the previously described loss of Fc gamma-RIII upon stimulation of the cells.
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PMID:Rapid increases in the membrane expression of neutral endopeptidase (CD10), aminopeptidase N (CD13), tyrosine phosphatase (CD45), and Fc gamma-RIII (CD16) upon stimulation of human peripheral leukocytes with human C5a. 168 87

Neuroblastoma (NB) is a solid tumor of childhood with a relatively bad prognosis, with the exception of young infants (less than 1 year), in whom spontaneous regression of tumor burden occurs. The reasons for this are still unknown but immune mechanisms may be involved. In this study, we have examined the ability of several monoclonal antibodies (MoAbs), which recognize markers predominantly expressed on human haematopoietic cells, to react with four human neuroblastoma cell lines (UKF-NB 1-4) and SK-N-SH as control cell line. In order to define the phenotype of NB cells, we used a large panel of MoAbs consisting of 2 major groups: a) well characterized MoAbs raised against antigens of neuroectodermal origin from the Kemshead-serie (e.g. UJ 13A, UJ 127.II, UJ 167.11, UJ 181.4, UJ 223.8, A2B5), b) monoclonal antibodies which have been considered to react with haematopoietic cells (HLA-DR and anti-CD-molecules CD1, CD7, CD9, CD10, CD13, CD16, CD19, CD20, CD24, CD57). The phenotypic analyses were performed at various times of culture by an immunoenzymatic procedure (APAAP-technique). Most of the MoAbs used against neuroblastoma cells showed a strong reactivity pattern with the NB cell lines. None of the antibodies against T-lymphocytes bound to any of the NB cells assayed in our study, with the exception of anti-CD 1. On the contrary, B-cell markers BA-2 (CD9) and BA-1 (CD24) cross-reacted with the NB cells just as well as the marker for NK-cells (CD57), but they did not express reactivity with Leu-11b (CD16), anti-CALLA (CD10) and anti-HLA-DR.
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PMID:Expression of markers shared between human haematopoietic cells and neuroblastoma cells. 238 85

Patients with myeloma have a depressed capacity to respond to antigenic challenge. Studies in this laboratory have previously described an unclassified lymphoid cell which binds human erythrocytes coated with human immunoglobulin G (IgG) anti-D antibody (EA) as important in the inhibition of Ig synthesis in myeloma patients. Using monoclonal antibodies, two-color fluorescence studies, and flow cytometry, we characterized this EA cell as a Leu-1+ (cluster designation (CD) 5), Leu-12+ (CD 19), Leu-16+ (CD 20), B2+ (CD 21), Leu-14+ (CD 22), and HLA-DR+ B cell. The cell was negative for antibodies to Leu-2 (CD 8), Leu-3 (CD 4), Leu-4 (CD 3), Leu-5 (CD 2), Leu-7, Leu-8, Leu-11 (CD 16), Leu-M1 (CD 15), Leu-M3, and CALLA (CD 10). This profile is consistent with a Leu-1+ B cell and excludes a T cell, natural killer cell, and monocyte. Comparison of the relative role of these cells to the role of monocytes in the suppression of pokeweed mitogen-stimulated Ig synthesis was determined in serial studies on 19 myeloma patients. The mean (+/- SEM) percentage of inhibition of Ig synthesis by monocytes from stage I myeloma patients was 14 +/- 2.2%, from stage II patients was 37 +/- 3.5%, and from stage III patients was 51 +/- 4.7%. Inhibition of Ig synthesis by Leu-1+ EA cells was 46 +/- 1.5%, 48 +/- 1.6%, and 43 +/- 3.7% in stage I, II, and III patients, respectively. Immunosuppressive B cells are an important component of inhibition of Ig synthesis in the immunodeficiency of myeloma.
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PMID:Multiple myeloma: an immunologic profile. IV. The EA rosette-forming cell is a Leu-1 positive immunoregulatory B cell. 295 12

In the present study, the expression of two NK-associated antigens (CD56 and CD16) together with six 'classically' considered lymphoid-related markers (TDT,CD19,CD10,CD7,CD2,CD4) has been analyzed by appropriate dual combinations in 265 acute myelogenous leukemia (AML) patients. Among the lymphoid markers, CD4 and CD7 were those most frequently expressed by AML blast cells (58% and 21.6%, respectively) while the incidence of positivity for the other markers was lower: CD19 (7.8%), CD10 (10.9%), CD2 (11.4%), and TDT (11.3%). Regarding NK-associated antigens, CD56 was present in 41% of AML cases analyzed whereas CD16 was detected in only 23%. All but one of the CD16+ cases coexpressed the CD56 antigen. The expression of these antigens was not associated with the degree of cell differentiation assessed either by morphological or immunophenotypical criteria, with the exception of the correlation observed between monocytic leukaemias and the expression of the CD4, CD56, and CD16 antigens. Regarding the prognostic value of the markers investigated, CD56 expression was associated with a tendency for a better outcome whereas CD7 was the only antigen that had an adverse influence on the survival of AML patients.
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PMID:Expression of NK and lymphoid-associated antigens in blast cells of acute myeloblastic leukemia. 750 72

We report a case of diffuse large-cell lymphoma which pursued a clinically indolent course while remaining untreated. The tumor cells expressed surface IgG, CD10, CD19 and CD20, but not surface IgM, IgD, IgA, CD5, CD16, CD32 and CD64. In addition, these cells appeared to coexpress kappa- and lambda-light chains on their surface. JH and J lambda genes were monoclonally rearranged, but not the J kappa gene. The present lymphoma was found to have arisen from follicle center cells expressing IgG lambda, while the surface kappa-light chain seemed to be extrinsic. Furthermore, the extrinsic immunoglobulin bearing the kappa-light chain may have belonged to IgG because no surface immunoglobulins other than IgG were detected on the cell surface. Then, the extrinsic IgG may have combined with certain molecules on the tumor-cell surface through its Fab portion because the tumor cells lacked all three receptors for the IgG-Fe portion. Fc gamma RI (CD64). Fc gamma RII (CD32) and Fc gamma RIII (CD16). From these findings and the patient's history of never having received a blood transfusion, we concluded that the present case might be of a B-cell lymphoma possibly coated with an IgG-type autoantibody which appeared to have anti-idiotypic activity.
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PMID:Localized diffuse large-cell lymphoma possibly coated with anti-tumor autoantibody: kappa lambda-dual-positive lymphoma. 911 2

Neutrophil surface molecules function in part as biological sensors. Surface antigens undergo several changes during neutrophilic maturation to accommodate the cell's function. Surface antigens may appear with neutrophilic maturation, such as CD16b, CD35, and CD10; disappear with maturation, such as CD49d and CD64; be maintained during maturation, such as CD32, CD59, and CD82; or disappear with maturation but reappear after neutrophilic extravasation, such as CD49b. This article reviews the alterations in surface antigen expression during normal neutrophilic granulopoiesis.
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PMID:Surface antigen changes during normal neutrophilic development: a critical review. 1206 21