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341 results on '"Carrel, S"'

7. Melanoma Immunology

Author

Bystryn, J. C., Kokoschka, E. M., Bröcker, E. B., Reisfeld, R., Ruiter, D. J., Vennegoor, C., Ferrone, S., Cesarini, J., Gaudry, H., Carrel, S., Giuffrè, L., Accolla, R., Isler, P., Zwadlo, G., Macher, E., Sorg, C., Luger, T. A., Köck, A., Vetterlein, M., Micksche, M., Gigli, I., Martin, D. E., Müller-Eberhard, H. J., Orfanos, Constantin E., editor, Stadler, Rudolf, editor, and Gollnick, Harald, editor

Published
1988
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10. Expression and Characterization of Leucocyte Antigens

Author

Allen, R., Ferrone, S., Hoch, J., Bankhurst, A., Spellmann, J., Burmester, G. R., Dimitriu-Bona, A., Gregersen, P., Waters, S. J., Winchester, R. J., Burrone, O. R., Calabi, F., Gilmore, D., Wright, B., Milstein, C., Clark, E., Martin, P., Hansen, J., Ledbetter, J., de Leij, L., Poppema, S., The, T. H., De Vries, J. E., Vaessen, R., Janssens, P., Tan, B., Heiman, A., Figdor, C. G., Dörken, B., Pfreundschuh, M., Moldenhauer, G., Schwarz, E., Hämmerling, G., Frisman, D., Baird, S., Gazit, E., Gothelf, Y., Gil, R., Orgad, S., Yunis, E. J., Girardet, Ch., Heumann, D., Mach, J.-P., von Fliedner, V., Carrel, S., Goyert, S. M., Silver, J., Hogg, N., Hokland, P., Schlossman, S. F., Ritz, J., Kalil, J., Abita, J. P., Chomienne, C., Poirier, O., Besluau, D., Dastot, H., Reboul, M., Fellous, M., Colombani, J., Kater, L., Brekelmans, P., Daemen, T., Schuurman, H. J., Katz, F., Povey, S., Stanley, K., Schneider, C., Greaves, M., Lemonnier, F. A., Le Bouteiller, P. P., Malissen, B., Golstein, P., Malissen, M., Mishal, Z., Caillol, D. H., Jordan, B. R., Kourilsky, F., Lennert, K., Stein, H., Miiller-Hermelink, H. K., Vollenweider, R., Karol, R. A., Eng, J., Dennison, D., Faris, E., Marcus, D. M., Piatier-Tonneau, D., Boyer, B., Debre, P., Charron, D., Reuben, J. M., Hersh, E. M., Mansell, P. W. A., Newell, G., Rios, A., Rumpold, H., Kraft, D., Förster, O., Schulz, T. F., Alsenz, J., Scheiner, O., Lambris, J., Dierich, M. P., Van Laarhoven, J. P. R. M., Broekhuizen, R., Spierenburg, G. Th., De Bruyn, C. H. M. M., Solbach, W., Röllinghoff, M., Wagner, H., Szer, I. S., Irani, A., Tax, W. J. M., Janossy, G., Jonker, M., Willems, R., Leeuwenberg, J., Capel, P. J. A., Koene, R. A. P., Leeuwenberg, H. F. M., Willems, H. M., Tetteroo, P. A. T., Visser, F., Landsdorp, P., von dem Borne, A. E. G. Kr., Thompson, J. S., Goeken, N. E., Brown, S. A., Rhoades, J. R., Yamamoto, K., Nakauchi, H., Karasuyama, H., Kitamura, K., Tanimoto, K., Okumura, K., Bernard, Alain, editor, Boumsell, Laurence, editor, Dausset, Jean, editor, Milstein, César, editor, and Schlossman, Stuart F., editor

Published
1984
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11. Leucocyte Malignancies

Author

Andrews, R. G., Bernstein, I. D., Torok-Storb, B., Bell, C. G., Biberfeld, P., Christensson, B., Öst, Å., Hast, R., Skoog, L., Andreason, R., Olsson, L., Lagerlöf, B., Reizenstein, P., Boucheix, C., Perrot, J. Y., Mirshahi, M., Fournier, N., Billard, M., Giannoni, F., Bernadou, A., Rosenfeld, C., Chiao, J. W., Wang, C. Y., Del Giacco, G. S., Cengiarotti, L., Di Tucci, A., Broccia, G., Corda, G., Mathieu, A., Indiveri, F., Locci, F., Mantovani, G., Detrick-Hooks, B., Boumsell, L., Bernard, A., Hooks, J. J., Divine, M., Farcet, J. P., Gourdin, M. F., Vasconcelos, A., Tabilio, A., Andre, C., Bouguet, J., Reyes, F., Fontan, S., Zabay, J. M., Garcia, M. C., Pascual-Salcedo, D., Campos, A., de la Concha, E. G., Gordon, J., Åman, P., Mellstedt, H., Klein, G., Habeshaw, J. A., Herrmann, F., Sieber, G., Rühl, H., Lebacq, A. M., Ravoet, A. M., Bazin, H., De Bruyere, M., Rodhain, J., Sokal, G., Losa, G., Maestroni, G., Lucivero, G., Antonaci, S., Stomeo, C., Bonomo, L., Magaud, J. P., Brochier, J., Vu Van, H., El Ansary, M., Gentilhomme, O., Bryon, P. A., Mathé, G., Minowada, J., Ogier, C., Ginsbourg, M., Goutner, A., Knapp, W., Canon, C., Melief, C. J. M., Miedema, F., Rümke, H. C., ten Berge, R. J. M., Terpstra, F. G., v.d. Borne, A. E. G. Kr., Willemze, R., v. Vloten, W., Miljkovic, A. K., Isakovic, K., Jankovic, B. D., Peng, R., Knowles, D. M., Bushkin, Y., Petrányi, G. G., Busch, G., Milford, E., Todd, R., Griffin, J., Reinherz, E., Terhorst, C., Schlossman, St., Carpenter, Ch., Richard, Y., Demeocq, F., Schwarting, R., Thoen, J., Førre, Ø. T., von Fliedner, V., Carrel, S., Heumann, D., Zaech, P., Sekaly, R. P., Girardet, Ch., Mach, J. P., Azzo, W., Worman, C., Mills, K., Brooks, D., Hogg, N., Zola, H., Beverly, P., Cawley, J., Bernard, Alain, editor, Boumsell, Laurence, editor, Dausset, Jean, editor, Milstein, César, editor, and Schlossman, Stuart F., editor

Published
1984
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12. Brain Tumor-Associated Antigens

Author

Carrel S, de Tribolet N, and Mach Jp

Subjects
Text mining, Antigen, business.industry, Brain tumor, medicine, Cancer research, Biology, medicine.disease, business
Published
2015

16. Stimulation of human T cells by streptococcal 'superantigen' erythrogenic toxins (scarlet fever toxins)

Author

Ma, Braun, Gerlach D, Udo Hartwig, Jh, Ozegowski, Romagné F, Carrel S, Köhler W, and Fleischer B

Subjects
Antigens, Bacterial, Scarlet Fever, Streptococcus pyogenes, Receptors, Antigen, T-Cell, alpha-beta, T-Lymphocytes, Immunology, Histocompatibility Antigens Class II, Immunoglobulin Variable Region, Exotoxins, Membrane Proteins, Lymphocyte Activation, Bacterial Proteins, Humans, Immunology and Allergy
Abstract

The pyrogenic (erythrogenic) exotoxins A and C (SPEA and SPEC) of Streptococcus pyogenes belong to the family of mitogenic toxins of which the staphylococcal enterotoxins are the prototypes. The erythrogenic toxin B (SPEB) is a proteinase precursor. All SPE have been reported to be superantigens. Here we have analyzed the human T cell response to these toxins. We used highly purified preparations of SPEA, SPEB, and SPEC from different S. pyogenes strains. These toxins were apparently homogenous in SDS-PAGE, IEF, and HPLC. In addition, recombinant SPEA and SPEC were produced in Escherichia coli. In cultures of PBMC, all three toxins expanded preferentially a fraction of T cells. Using mAb against V beta 2, -5, -6, -8, and -12, we investigated the phenotype of the stimulated cells. Natural SPEA, SPEB, and SPEC strongly stimulated V beta 8+ T cells, whereas recombinant SPEA and SPEC did not. Both natural and recombinant SPEA stimulated V beta 12+ cells and both natural and recombinant SPEC stimulated V beta 2+ cells. In accordance with these findings, a human V beta 8+ line responded to all three toxins derived from S. pyogenes but not to the recombinant proteins. An antiserum against natural SPEC neutralized specifically the V beta 2-stimulating activity of SPEC and the V beta 8-stimulating activity of all three toxins, but had no effect on the response to other superantigens. This shows that trace amounts of a potent novel V beta 8-stimulating activity not identical to SPEA and SPEC are responsible for the stimulation of V beta 8+ T cells by natural SPEA and SPEC reported previously. In a preliminary screening of S. pyogenes strains from patients, we found that this novel superantigen appears to be more widely distributed than SPEA and SPEC. Furthermore, we present evidence that also the superantigenic properties of SPEB are due to contaminations with this V beta 8 stimulator. The response to SPEB usually required 1000 times higher concentrations than to SPEA or SPEC. Antisera to SPEC but not to SPEB inhibited the response of PBMC and V beta 8+ Jurkat cells to SPEB. Furthermore, more stringent purification of SPEB yielded SPEB preparations devoid of mitogenic activity. These results indicate that the mitogenicity that is commonly attributed to SPEB is due to minute contaminations of the V beta 8 stimulator. These results raise two important caveats for the work with these highly potent T cell mitogens.(ABSTRACT TRUNCATED AT 400 WORDS)

Published
1993

24. Letter to the editor

Author

Pedro Romero, Carrel S, and Donata Rimoldi

Subjects
Cancer Research, Text mining, Oncology, Antigen, business.industry, Cancer research, Encoding (semiotics), Human melanoma, Biology, business, Gene
Published
1993

27. Human melanoma cells express a functional interleukin-2 receptor

Author

Plaisance, S., primary, Rubinstein, E., additional, Alileche, A., additional, Han, D. S., additional, Sahraoui, Y., additional, Mingari, M. C., additional, Bellomo, R., additional, Rimoldi, D., additional, Colombo, M. P., additional, Jasmin, C., additional, Carrel, S., additional, and Azzarone, B., additional

Published
1993
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41. Neoplastic meningitis in malignant melanoma: diagnosis with monoclonal antibodies.

Author

Moseley, R P, Davies, A G, Bourne, S P, Popham, C, Carrel, S, Monro, P, and Coakham, H B

Abstract

Six patients with neoplastic melanomatous meningitis were studied. The diagnosis of this complication of malignant disease rests on the demonstration of malignant cells within the CSF. The addition of monoclonal antibody immunocytology to conventional techniques significantly improved the diagnostic sensitivity of CSF cytology, allowing for earlier and therefore more effective palliative treatment. [ABSTRACT FROM AUTHOR]

Published
1989

42. Heterogeneity of T cell receptor idiotypes in rheumatoid arthritis.

Author

Brennan, F. M., Allard, S., Londei, M., Savill, C., Boylston, A., Carrel, S., Maini, R. N., and Feldmann, M.

Subjects
RHEUMATOID arthritis, T cells, CELL receptors, SYNOVIAL membranes, BLOOD, JOINT diseases
Abstract

The nature of the T cell response in the rheumatoid synovium was investigated by using monoclonals MX9 and 42/lCl, which recognize the Vβ8 and Vβ5 T cell receptor gene families respectively. The blood and synovial T cells of ten patients with rheumatoid arthritis were compared. The majority (8/10) had different numbers of Vβ5 and Vβ8 cells in the joints from those in the blood, indicating that the T cells in the joints were not a sample of those in the blood. In three patients both Vβ5 and Vβ8 cells in the joint were augmented in number, suggesting that the T cells selectively retained in the joint were not members of a single clone, but derived from many clones. Some patients had increased levels of Vβ5 or Vβ8 alone in the joint indicating that heterogeneity existed between patients. These results are not consistent with the preferential or dominant use of a single Vβ gene family in the T cells involved in the rheumatoid arthritic joints. [ABSTRACT FROM AUTHOR]

Published
1988

49. Regulation of clonal growth by anti-T-cell receptor antibody-directed lysis.

Author

De Berardinis, P., Londei, M., Carrel, S., and Feldmann, M.

Subjects
T cells, IMMUNOGLOBULINS, LYMPHOCYTES, MONOCLONAL antibodies, CELL receptors, CLONE cells
Abstract

CD4 and CD8 T-cell clones were generated using the Mx9 monoclonal antibody (mAb), which recognizes the Vβ8 T-cell receptor (TcR) gene family. The interaction of these clones with the Mx9 antibody was analysed and all were found to be specifically stimulated to proliferate by plastic- adherent Mx9. In the presence of Mx9 or its F(ab')2 fragment, CD8+Mx9+ clones were capable of specifically lysing the CD4 + Mx9-T-cell clones. No lysis was seen of Mx9+ T-cells, or in the absence of the antibody. Conversely CD4 Mx9+ cells did not have lytic function. These results indicate that cross-linking of T cells via their antigen-specific receptors may initiate a unidirectional killing. Unlike previously reported lytic systems involving anti-TcR antibodies (e.g. anti-CD3), these results suggest that this mechanism may have an important physiological role in immune regulation. Antis idiotypic antibodies have been shown to recognize T-cell receptors. These may exert profound immunosuppressive effects by inducing the lysis of the helper cells or B cells. [ABSTRACT FROM AUTHOR]

Published
1988

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