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

Expression of decay-accelerating factor (DAF or CD55) and of CD59 during hematopoietic cell development in normal bone marrow and on peripheral blood leukocytes were characterized by three-color immunofluorescence experiments. With this technique cell subsets were identified by forward light scatter, orthogonal light scatter, and two cell-surface antigens. For each cell lineage, specific combinations of two monoclonal antibodies labeled with different fluorochromes were used. DAF or CD59 were then quantitated on the defined cell subsets from the fluorescence signal of the respective antibody conjugated with a third fluorochrome. Early uncommitted hematopoietic progenitor cells (CD34+, CD38-) all expressed both proteins homogeneously. Initial commitment to the erythroid (CD71+, CD45dim), myeloid (CD33+), or B lymphocyte (CD10+) lineages was not associated with changes in DAF or CD59 levels. With erythroid development, i.e., after loss of CD45 and decrease of CD71, expression of both proteins decreased. With myeloid maturation, expression of CD59 remained constant and expression of DAF varied. During neutrophil maturation, DAF decreased initially and then reemerged on maturing neutrophils concurrently with the appearance of CD16 (Fc gamma RIII), whereas during monocyte maturation, DAF increased concurrently with up-regulation of CD14. With B cell development, expression of DAF increased concurrently with down-regulation of CD10 and up-regulation of CD20, whereas expression of CD59 diminished slightly late in B cell maturation. Analysis of peripheral blood elements showed that monocytes, neutrophils, and B lymphocytes expressed both proteins homogeneously, but that in contrast to other cell subsets, which all expressed CD59, only a subset of (CD3+) T lymphocytes and (CD16+) Natural killer cells expressed DAF. The absence of DAF was not related to CD4 or CD8 expression or to the presence of activation markers (CD25+, CD38+), memory cell markers (CD58+, CD45RO+), or virgin T cell markers (CD45RA+), but was correlated with expression of CD11b (CR3) and CD11c (gp150/95). Although CD21+ (CR2) and CD35+ (CR1) cells all expressed DAF, CD11a (LFA-1) levels correlated inversely with those of DAF. Although the presence of CD55 and CD59 on early progenitor cells and throughout hematopoietic cell development is consistent with the requirements for both proteins in protection of host cells from complement-mediated injury, the physiological relevance of the unique patterns of variation for each cell lineage is unclear. Nevertheless, the availability of a detailed DAF and CD59 expression map in normal marrow will facilitate analyses of alterations during hematopoietic development that may occur in hematological disorders including paroxysmal nocturnal hemoglobinuria (PNH).
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PMID:Expression of the DAF (CD55) and CD59 antigens during normal hematopoietic cell differentiation. 128 89

Using an indirect immunoperoxidase technique, we tested frozen specimens from 12 Wilms' tumors with monoclonal antibodies (MoAbs) reacting against a large panel of molecules including laminin, fibronectin, cytokeratin, vimentin, villin, CD24, CALLA/CD10, CR1, CD26, class I and class II major histocompatibility complex (MHC) molecules, and endothelium factor VIII. These molecules were chosen because they are markers of specific segments of the mature kidney and because their loss or acquisition is indicative of different steps of human nephrogenesis. KI67 MoAb was used to evaluate the proliferating activity of the cells. The blastemal component (cell compact areas) of Wilms' tumors consisted of vimentin-positive cells with a fibronectin network. However, signs of epithelial maturation were present in compact areas where cytokeratin-positive cells producing laminin were observed. The cells exhibited a high degree of proliferating activity. The tubule formations consisted of cytokeratin-positive cells and had a defined laminin border. All the cells, whether in compact areas or in tubules, were strongly CD24-positive. Some tubular formations showed signs of proximal maturation with the presence of CALLA, CD26, and even villin. In four cases class I-MHC molecules were expressed by some tubular cells. Large cystic cavities present in five cases were edged by cytokeratin, CD24-positive cells, or by vimentin, CALLA, CR1-positive cells. Some glomeruloid bodies, present in two cases, were also composed of vimentin, CALLA, and CR1-positive cells which correspond to the mature podocyte phenotype. The interstitial tissue contained mainly laminin and fibronectin network with macrophages and few CD3 lymphocytes. The presence of large cells with muscular differentiation was noted; round vimentin and CD26-positive cells were also seen. The endothelial cells of the vessels exhibited vimentin, factor VIII, and class I and class II MHC molecules as do mature cells, but in some cases the endothelial cells lacked class II molecule expression and were CALLA-positive. These results which confirmed and extended those previously described show that cell differentiation in Wilms' tumor mimics that observed during metanephros development. Moreover, this study shows that tumoral cells in nephroblastoma share several antigens with cells from lymphoid lineage (CD24, CALLA, and CD26) as do developing and mature kidney cells. Such cell phenotype dissection provides a useful and reliable tool for testing the influence of various factors on the development of hetero-transplanted or cultured Wilms' tumors.
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PMID:Cell differentiation in Wilms' tumor (nephroblastoma): an immunohistochemical study. 169 63

Using an indirect immunoperoxidase technique, we tested frozen specimens from one Wilms' tumour composed of numerous glomeruloid bodies devoid of blood vessels, with monoclonal antibodies directed against vimentin, cytokeratin, CALLA/CD10, CD24, CR1/CD35, endothelium factor VIII, class I and II MHC molecules, laminin, fibronectin, and non-collagenic domain NC1 of type IV collagen. Two reagents against Goodpasture determinants were used: P1 monoclonal antibody and serum IgG (GP antibodies) from a biopsy-proven Goodpasture patient. Glomeruloid bodies comprised two cell types: a peripheral layer of parietal epithelial cells (cytokeratin and CD24-positive) and central cell clumps of podocytes (vimentin and CALLA-positive). The basal lamina surrounding the glomeruloid bodies contained laminin and NC1 domain of type IV collagen, while that present between the podocytes reacted strongly with laminin, and P1 and GP antibodies. Endothelium factor VIII was not detected within the glomeruloid bodies and CR1 molecules bound to the basement membrane material within them. These data favour the hypothesis that podocytes produce the basement membrane material which bears Goodpasture determinants recently identified as a novel chain, named the alpha 3 chain, of type IV collagen.
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PMID:Deduction from Wilms' tumour that glomerular podocytes produce the basement membrane material bearing Goodpasture determinants. 196 93

Human cell lines (the T-cell lines H9, Jurkat, and HUT102, the myeloid lines U937 and HL60, and the Raji B cell line) were infected with HIV-1. HIV-1 antigen could be detected by immunofluorescence analysis in more than 50% of T cells and myeloid cells 15 days after infection. Infection of Raji cells took more than 2-3 months. Studies of cell surface marker expression revealed remarkable changes after HIV-1 infection of Raji cells: expression of CR2 (C3d/EBV receptor, CD19, CD20, CD22, CD23, CD10, and surface IgM) were highly reduced, in the case of CR2 and membrane-IgM from 100 to 0%, whereas levels of CD37 and CD38 remained unaltered by HIV-1 infection. U937 cells showed a reduction of CD4 expression from 14 to 5% after HIV-1 infection; the CR3 expression slightly increased from 25 to 30%. In contrast, HLA-DR was only expressed (21%) after HIV-1 infection but not in uninfected U937 cells. Expression of HLA-DR could be detected also in HL60 cells (33%) after HIV-1 infection. In H9 cells, CD4 was reduced from 60 to 30% after HIV-1 infection, whereas HLA-DR and CD25/IL-2 receptor expression increased from 16 to 90% and from 0 to 50%, respectively. CD4 was reduced from 70 to 0% from Jurkat cells after HIV-1 infection, whereas expression of CR2 was only slightly diminished from 8 to 4%. Expression of CR1 and HLA-DR was slightly increased in these cells (1 to 3%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression of the C3d/EBV receptor and of other cell membrane surface markers is altered upon HIV-1 infection of myeloid, T, and B cells. 213 11

The correlation between expression of differentiation antigens and morphogenesis was examined in 11 human nephroblastomas using monoclonal antibodies which recognize both hemopoietic and renal cells. Analysis of frozen tissue sections by indirect immunofluorescence revealed that blastema cells and some tubules were recognized by BA-1 and OKB2, which identify unstimulated B cells and granulocytes. Stroma, some tubules, and focal blastema were recognized by BA-2, which identifies a 24-kDa antigen on leukemic cells and platelets. Mature epithelium in glomerular bodies was identified by C3bR and J5, which recognize CR1 and the common acute lymphoblastic leukemia antigen, respectively. Tissue sections from a clear cell sarcoma and a mesoblastic nephroma were notably reactive only with BA-2. These observations demonstrate that the relationship between antigen expression and morphology in nephroblastomas is similar to that observed in fetal kidney and suggest that expression of these cell surface antigens may have a role in morphogenesis.
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PMID:Cellular antigens in nephroblastoma: identification with monoclonal antibodies which recognize hemopoietic cells. 303 May 90

Ontogenesis of the glomerular C3b receptor (CR1) was studied in kidneys from 16 fetuses aged from 9 to 32 weeks, using immunohistochemical techniques and the F(ab')2 fragment of a monospecific rabbit antibody to CR1, and adherence of C3b-coated sheep erythrocytes. By indirect immunofluoresence, anti-CR1 stained presumptive glomerular epithelium from the end of the S-body stage of nephron differentiation. Staining increased with visceral epithelial cell proliferation and with differentiation of the nephron from the subcortical to the juxtamedullary part of the fetal kidney. Using electron microscopy and an indirect immunoperoxidase technique, CR1 antigen was detected on the plasma membrane in the basolateral part of primitive podocytes from the late S-body stage, following the acquisition by podocytes of the capacity to synthetize a basal lamina. Endothelial cells and mesangial cells did not stain for CR1 antigen. CR1 antigen was expressed by podocytes from the same stage of glomerular differentiation as was the CALLA antigen. Glomerular expression of CR1 on podocytes preceded that of Ia on glomerular endothelial cells. C3b-bearing sheep erythrocytes only adhered to clover-like lobulated glomeruli at a late stage of glomerular differentiation. Glomerular CR1, a specific marker of glomerular capillary epithelial cells is one of the earliest markers expressed by resident glomerular cells during renal ontogenesis.
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PMID:Ontogenesis of the glomerular C3b receptor (CR1) in fetal human kidney. 316 74

In the past few years, we have learned a great deal about the biologic function of structures bearing blood group antigens. Some blood group antigen-bearing proteins function as major transport channels within the erythrocyte membrane; these include the anion transporter (band 3: Diego and Wright antigens), the water channel (aquaporin: Colton antigens), and the urea transporter (Kidd antigens). At least two erythrocyte blood group antigen proteins have complement regulatory functions: the complement receptor type 1 (CR1, CD35: Knops antigens) and decay accelerating factor (DAF, CD55: Cromer antigens). Some blood group antigens reside on proteins with known receptor functions, such as the chemokine receptor (Duffy) and the hyaluronan receptor (Indian). The Cartwright antigens reside on an enzyme, acetylcholinesterase, and the Kell antigens reside on a protein that belongs to the CALLA-related family of neutral metalloproteinases. Finally, some blood group antigens reside on proteins that serve crucial structural functions necessary to normal erythrocyte lifespan and morphology. These proteins include band 3, glycophorins C/D (bearing the Gerbich antigens), and the Rh proteins. Both oligosaccharide and protein blood group antigens may act as receptors for bacterial, viral, and parasitic infectious agents.
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PMID:Biologic functions of blood group antigens. 937 20

Neprilysin (NEP, CD10, CALLA-common acute lymphoblastic leukaemia antigen, neutral endopeptidase, enkephalinase) is a zinc-dependent metallopeptidase, which is the first podocytic antigen, which has been shown to induce human membranous glomerulonephritis (GN). Debiec et al. in a case of antenatal membranous GN identified NEP as the podocyte target antigen of circulating antibodies produced by the mother who failed to express NEP on granulocytes. However, NEP is expressed on normal podocytes and renal proximal tubular epithelial cells. Moreover, decreased podocyte expression of NEP has been found in a variety of glomerular diseases. Recent studies show that in patients with GN the podocyte expression of NEP correlates with that of other podocyte proteins, i.e.: synaptopodin and CR1 and reflects the severity of glomerular damage.
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PMID:[The involvement of neprilysin in the pathogenesis of glomerulopathies]. 1982 39

Podocytes are considered as the most important cells that determine loss of structure and function of the glomerular filter. We compared the expression of three podocyte markers, i.e.: synaptopodin (SYN), CR1 and neprilysin (NEP) in 107 patients with different forms of glomerulonephritis (GN) and 5 normal kidneys (NK). A quantitative immunohistochemistry was applied to evaluate the expression of podocyte proteins. The results were related with serum creatinine (Scr), estimated glomerular filtration rate (eGFR) and urinary protein. We observed the reduction in the podocyte expression of NEP, SYN and CR1 in proliferative and non-proliferative forms of GN. Interestingly, in mesangial proliferative GN (MesPGN), the expression of SYN and CR1 was lower in IgA-MesPGN than in non-IgA-MesPGN (p<0.005 and p<0.02, respectively). In all the patients, the expression of NEP and SYN was positively related (r=0.53, p=0.02) as that of NEP and CR1 (r=0.39, p=0.04). Yet, clinical correlations with Scr (r=-0.33, p=0.03) and eGFR (r=0.26, p=0.05) were obtained only with respect to CR1. In conclusion, SYN, CR1 and NEP may be used as markers of podocyte loss in patients with GN. However, in agreement with previous studies, the clinical relevance draws a special attention to the expression of CR1.
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PMID:The Comparison of the Podocyte Expression of Synaptopodin, CR1 and Neprilysin in Human Glomerulonephritis: Could the Expression of CR1 be Clinically Relevant? 2367 11