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8. Progress in Experimental Systemic Active Immunotherapy of Cancer

Author

Mathé, G., Florentin, I., Bruley-Rosset, M., Kiger, N., Allfrey, V. G., editor, Allgöwer, M., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Della Porta, G., editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Kirsten, W. H., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Macbeth, R. A., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, Senn, H. J., editor, Mathé, Georges, editor, and Muggia, Franco M., editor

Published
1980
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9. In Vivo Immunomodulating Properties of Two Synthetic Agents: Azimexon and Tuftsin

Author

Florentin, I., Schulz, J., Bruley-Rosset, M., Kiger, N., Martinez, J., Mathé, G., Allfrey, V. G., editor, Allgöwer, M., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Della Porta, G., editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Kirsten, W. H., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Macbeth, R. A., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, Senn, H. J., editor, Mathé, Georges, editor, and Muggia, Franco M., editor

Published
1980
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10. Correction of Immunodeficiency in Aged Mice by Levamisole and Bestatin Administration

Author

Bruley-Rosset, M., Florentin, I., Kiger, N., Schulz, J. I., Mathé, G., Allfrey, V. G., editor, Allgöwer, M., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Della Porta, G., editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Kirsten, W. H., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Macbeth, R. A., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, Senn, H. J., editor, Mathé, Georges, editor, and Muggia, Franco M., editor

Published
1980
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11. Third Generation of Systemic Adjuvants of Immunity: Experimental Basis for Adjuvant Combinations

Author

Mathé, G., Florentin, I., Schulz, J. I., Bruley-Rosset, M., Kiger, N., Allfrey, V. G., editor, Allgöwer, M., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Porta, G. Della, editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Kirsten, W. H., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Nakahara, W., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Taylor, R. M., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, Bonadonna, Gianni, editor, Mathé, Georges, editor, and Salmon, Sydney E., editor

Published
1979
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12. Serum Leukocyte Inhibitory Factor in Cancer Patients (Serum LIF)

Author

Fassas, A., Bruley-Rosset, M., Allfrey, V. G., editor, Allgöwer, M., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Della Porta, G., editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Kirsten, W. H., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Nakahara, W., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Taylor, R. M., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, Bonadonna, Gianni, editor, Mathé, Georges, editor, and Salmon, Sydney E., editor

Published
1979
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13. Treatment of Murine EAkR Lymphosarcoma by Surgery Combined With Systemic or Local Active BCG Immunotherapy Applied Repeatedly

Author

Economides, F., Bruley-Rosset, M., Mathé, G., Allfrey, V. G., editor, Allgöwer, M., editor, Bauer, K. H., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bocke, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Della Porta, G., editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Kirsten, W. H., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Nakahara, W., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Taylor, R. M., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, and Mathé, Georges, editor

Published
1977
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14. Effects of the Removal of the Regional Lymph Nodes on the Survival of Mice Bearing B16 Melanoma or EAkR Lymphosarcoma

Author

Economides, F., Bruley-Rosset, M., Allfrey, V. G., editor, Allgöwer, M., editor, Bauer, K. H., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bocke, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Della Porta, G., editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Kirsten, W. H., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Nakahara, W., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Taylor, R. M., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, and Mathé, Georges, editor

Published
1977
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15. Lymphocyte-Macrophage Interactions in BCG-Treated Mice

Author

Florentin, I., Bruley-Rosset, M., Davigny, M., Allfrey, V. G., editor, Allgöwer, M., editor, Bauer, K. H., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Della Porta, G., editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Hamperl, H., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Nakahara, W., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Taylor, R. M., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, Mathé, Georges, editor, Florentin, Irène, editor, and Simmler, Marie-Christine, editor

Published
1976
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17. Three New Agents for Immunotherapy Trials: Azimexon, Bestatin, and Tuftsin

Author

Mathé, G., Florentin, I., Bruley-Rosset, M., Goutner, A., Serrou, B., Allfrey, V. G., editor, Allgöwer, M., editor, Berenblum, I., editor, Bergel, F., editor, Bernard, J., editor, Bernhard, W., editor, Blokhin, N. N., editor, Bock, H. E., editor, Braun, W., editor, Bucalossi, P., editor, Chaklin, A. V., editor, Chorazy, M., editor, Cunningham, G. J., editor, Porta, G. Della, editor, Denoix, P., editor, Dulbecco, R., editor, Eagle, H., editor, Eker, R., editor, Good, R. A., editor, Grabar, P., editor, Harris, R. J. C., editor, Hecker, E., editor, Herbeuval, R., editor, Higginson, J., editor, Hueper, W. C., editor, Isliker, H., editor, Kieler, J., editor, Kirsten, W. H., editor, Klein, G., editor, Koprowski, H., editor, Koss, L. G., editor, Macbeth, R. A., editor, Martz, G., editor, Mathé, G., editor, Mühlbock, O., editor, Old, L. J., editor, Potter, V. R., editor, Sabin, A. B., editor, Sachs, L., editor, Saxén, E. A., editor, Schmidt, C. G., editor, Spiegelman, S., editor, Szybalski, W., editor, Tagnon, H., editor, Tissières, A., editor, Uehlinger, E., editor, Wissler, R. W., editor, Rentchnick, P., editor, Senn, H. J., editor, Bonadonna, G., editor, and Salmon, S., editor

Published
1982
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28. The J alpha segment contributes to the affinity of V beta 6+ cells for vSAG-7 (Mls-1a) presented by I-A molecules

Author

Churaqui, E, Oukka, M, Tilloy, F, Mayadoux, E, Bruley-Rosset, M, and Kosmatopoulos, K

Subjects
Superantigens, Base Sequence, Receptors, Antigen, T-Cell, alpha-beta, T-Lymphocytes, Molecular Sequence Data, Dose-Response Relationship, Immunologic, Histocompatibility Antigens Class II, Immunoglobulin Variable Region, Antibodies, Monoclonal, chemical and pharmacologic phenomena, Mice, Inbred Strains, Clone Cells, Mice, Animals, Immunoglobulin Joining Region, Amino Acid Sequence, Gammaretrovirus, Cell Division, Research Article
Abstract

Recognition of superantigens (SAG) by T cells is major histocompatibility complex (MHC) dependent but not MHC restricted. In the case of vSAG-7 (Mls-1a), encoded by the Mtv-7 provirus, I-E molecules play a dominant role in the vSAG-7-MHC-T-cell receptor (TCR) interaction, the I-A molecule being less important. vSAG-7 is recognized predominantly by T cells bearing the V beta 6 element, which are deleted in Mtv-7+ mice; this deletion is nearly complete in mice expressing I-E molecules, but only partial in mice expressing exclusively the I-A molecules of permissive haplotypes. In view of these data, we hypothesized that vSAG-7-specific V beta 6+ T cells have a large spectrum of affinities for the MHC-vSAG-7 complex and that all of them, even those with a relatively low affinity, recognize the I-E-vSAG-7 complex, while only those with high affinity can recognize the I-A-vSAG-7 complex. Fourteen CD4 V beta 6+ vSAG-7-specific clones were studied and classified into three groups of avidity, depending on their interactions with different I-E- I-A(+)-vSAG-7 permissive haplotypes. Sequencing of the alpha and beta chains of their TCR suggested that the affinity for the vSAG-7 is influenced by the J alpha element. Four out of six low-affinity T-cell clones possessed the transcript for the J alpha 34 segment. Furthermore, five out of six low-affinity T-cell clones had the GGSN sequence in their CDR3 alpha, while the sixth low affinity clone had the conservative substituted SGGN sequence. These results strongly suggest that the expression of the J alpha 34 segment confers a very weak reactivity to T cells recognizing vSAG-7.

Published
1995

39. CD8+ cytotoxic T cell repertoire implicated in graft-versus-leukemia effect in a murine bone marrow transplantation model.

Author

de La Selle, V, Riché, N, Dorothé, G, and Bruley-Rosset, M

Subjects
LEUKEMIA, BONE marrow transplantation
Abstract

In our model of murine BMT, the lethal GVHD which develops against DBA/2 host incompatible minor histocompatibility antigens (mHAgs) can be prevented by donor preimmunization before grafting. Recipient mice become long survivors (LS mice) and tolerant to host mHAgs. However, a GVL effect is preserved and mediated by CD8+ CTL able to kill P815 tumor cells in vitro and in vivo. To explain why a GVL exists without GVHD, we compared the CTL activity of LS and B10.D2 donor mice after immunization with DBA/2 spleen cells or with P815 cells. Experimental results indicated that: (1) the level of cytotoxicity for H-2b incompatible cells was similar in LS and B10.D2 mice; (2) CTL recognizing host DBA/2 mHAgs, whose expression is restricted to the spleen or is shared between spleen and P815 cells, were partially unresponsive in LS mice; (3) P815 injection into LS mice predominantly generated CTL specific for antigens restricted to P815 cells, the repertoire of which was not tolerized. Characterization of TCR βchain showed that the diversity of Vβand Jβusage by CD8+ T cells activated after P815 injection is considerably restricted in LS mice, compared to B10.D2 donor mice. These results indicated that the GVL effect in LS mice involved mainly T cells specific for tissue-restricted antigens expressed on P815 cells and not on normal DBA/2 spleen cells. In addition, the absence of GVHD may be attributed to the unresponsiveness of CD8+ CTL specific for host mHAgs expressed on DBA/2 spleen cells. [ABSTRACT FROM AUTHOR]

Published
1999
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40. Study of the effect of single or multiple doses of BCG on antibody-dependent cellular cytotoxicity.

Author

Kiger, N., Bruley-Rosset, M., Huchet, R., and Mathe, G.

Subjects
*CELL-mediated cytotoxicity, *BCG vaccines, *BLOOD cells, *MACROPHAGES, *KILLER cells, *IMMUNE response
Abstract

The in vivo effects of BCG were studied on antibody-dependent cellular cytotoxicity (ADCC) using an assay in which the effectors were spleen cells of BCG-treated mice, and the targets antibody-coated chicken red blood cells (CRBC). In the study of the time course of action, an increased ADCC-activity was observed starting at day 10 with a maximum (four-fold augmentation) at day 14 after BCG treatment. The nature of the effector cell was investigated: in normal mice the activity was found in two cell populations, i.e. macrophages and theta-negative (θ-) nylon-adherent spleen cells. A BCG treatment increased the ADCC activity of macrophages of θ- nylon-adherent spleen cells and induced a population of θ- nylon-non-adherent spleen cells. In old mice, the effects of BCG were compared after a weekly long-term (6 months) treatment and after administration of a single dose. It was concluded that ADCC is higher in old mice than in young mice and can be further increased by treatment with a single dose of BCG in contrast with the long-term treatment which impaired this immune reaction. [ABSTRACT FROM AUTHOR]

Published
1980

41. Restoration of impaired immune functions of aged animals by chronic bestatin treatment.

Author

Bruley-Rosset, M., Florentin, I., Kiger, N., Schulz, J., and Mathé, G.

Subjects
*BESTATIN, *IMMUNOLOGICAL adjuvants, *DRUG administration, *SUPPRESSOR cells, *IMMUNOSUPPRESSION, *IMMUNOLOGY
Abstract

An attempt to correct the state of immunodeficiency in old age was made by repeatedly injecting a chemically defined immunostimulating agent, bestatin, to 16 month old (C57B1/6 × BALB/c) F1 mice. Aged mice were found to have depressed T-cell and B-cell responses but increased ADCC activity. Weekly injections of bestatin over a period of 6 months resulted in varying effects depending on the dose administered. Small doses (10 μg per injection) were more effective m restoring humoral responses to SRBC rather than delayed-type hypersensitivity reactions, whereas large doses (100 μg per injection) acted in the opposite way. Macrophage activation was only obtained after the administration of the high doses of bestatin. Continuous treatment with bestatin did not prevent the appearance of suppressor cells induced by ageing. It led to a significant reduction of ADCC activity in aged animals near to the base line value of young animals. Animals were examined for the presence of spontaneous tumours from the end of the treatment until the age of 28 months. A significant reduction of spontaneous turnout incidence was observed in mice given repeated injections of 100 μg bestatin when compared to untreated aged mice and to mice given the low doses of bestatin. [ABSTRACT FROM AUTHOR]

Published
1979

46. Relative importance of CD4+ and CD8+ T cell repertoires in the development of acute graft-versus-host disease in a murine model of bone marrow transplantation.

Author

Miconnet, I, de La Selle, V, and Bruley-Rosset, M

Subjects
GRAFT versus host disease, T cells, CD antigens, BONE marrow transplantation
Abstract

T cell repertoire alterations occurring after allogeneic BMT and related emergence of aGVHD has not been directly demonstrated. CD4, CD8 and Vβ usage of T cells infiltrating spleen, lymph nodes and liver was compared in lethally irradiated F1(DBA/2 × B10.D2) recipients which develop (GVHD mice) or not (long survivor:LS mice) aGVHD across minor histocompatibility antigens (mHAgs) and Mtv-6 and Mtv-7 encoded superantigens (SAgs) barriers according to experimental conditions. The early expansion in GVHD mice of CD4Vβ6+ and of CD4Vβ3+ T cell subsets specific for Mtv-7 and Mtv-6 SAgs, respectively, is abolished in LS protected mice. By contrast, CD8+ T cells infiltrate lymph nodes, the liver but not the spleen of LS as in GVHD mice. Vβ subset overexpression is frequent in all T cell phenotypes in GVHD but only among CD8+ T cells in LS mice. Predominant Vβ pattern subpopulation is unique to each mouse. Overexpressed Vβ subpopulation sequencing clearly indicates that expansion results from a very limited number of clones. Association of a given Vβ segment with different Jβ for each mouse suggests that the response is directed towards many different antigens. The data emphasize that Mtv-SAg and mHAgs CD4+ T cells are of crucial importance during GVHD and that there is no relationship between CD8+ T cell repertoires and pathological status. [ABSTRACT FROM AUTHOR]

Published
1998
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47. The Jα segment contributes to the affinity of Vβ6+ cell for vSAG-7 (M1s-1a) presented by I-A molecules.

Author

Churaqui, E., Oukka, M., Tilloy, F., Mayadoux, E., Bruley-Rosset, M., and Kosmatopoulos, K.

Subjects
IMMUNE recognition, IMMUNE response, IMMUNOSPECIFICITY, SUPERANTIGENS, MAJOR histocompatibility complex, T cells
Abstract

Recognition of superantigens (SAG) by T cells is major histocompatibility complex (MHC) dependent but not MHC restricted. In the case of vSAG-7 (Mls-1a), encoded by the Mtv-7 provirus, I-E molecules play a dominant role in the vSAG-7-MHC-T-Cell receptor (TCR) interaction, the I-A molecule being less important, vSAG-7 is recognized predominantly by T cells bearing the Vβ6 element, which are deleted in Mtv-7+ mice; this deletion is nearly complete in mice expressing I-E molecules, but only partial in mice expressing exclusively the I-A molecules of permissive haplotypes. In view of these data, we hypothesized that vSAG-7-specific Vβ6+ T cells have a large spectrum of affinities for the MHC-vSAG-7 complex and that all of them, even those with a relatively low affinity, recognize the I-E-vSAG-7 complex, while only those with high affinity can recognize the I-A-vSAG-7 complex. Fourteen CD4 Vβ6+ vSAG-7-specific clones were studied and classified into three groups of avidity, depending on their interactions with different I-E- I-A+-vSAG-7 permissive haplotypes. Sequencing of the α and β chains of their TCR suggested that the affinity for the vSAG-7 is influenced by the Jα element. Four out of six low affinity T-cell clones possessed the transcript for the Jα34 segment. Furthermore, five out of six Iow-affinity T-cell clones had the GGSN sequence in their CDR3α, while the sixth low affinity clone had the conservative substituted SGGN sequence. These results strongly suggest that the expression of the Jα34 segment confers a very weak reactivity to T cells recognizing vSAG-7. [ABSTRACT FROM AUTHOR]

Published
1995

48. Leukocyte migration-inhibitory activity in serum from patients with aplastic anemia

Author

Bruley-Rosset M and Fassas A

Subjects
Adult, Leukocyte migration, Lymphokines, Leukemia, Adolescent, business.industry, Anemia, Aplastic, General Medicine, Middle Aged, medicine.disease, Inhibitory postsynaptic potential, Prognosis, Child, Preschool, Immunology, medicine, Humans, Aplastic anemia, business, Child, Aged
Published
1979

49. Study of the effect of single or multiple doses of BCG on antibody-dependent cellular cytotoxicity

Author

Kiger, N, Bruley-Rosset, M, Huchet, R, and Mathe, G

Subjects
Aging, Erythrocytes, Macrophages, T-Lymphocytes, Antibody-Dependent Cell Cytotoxicity, Dose-Response Relationship, Immunologic, chemical and pharmacologic phenomena, Mice, Inbred Strains, Cell Separation, Kinetics, Mice, BCG Vaccine, Cell Adhesion, Animals, Female, Spleen, Research Article
Abstract

The in vivo effects of BCG were studied on antibody-dependent cellular cytotoxicity (ADCC) using an assay in which the effectors were spleen cells of BCG-treated mice, and the targets antibody-coated chicken red blood cells (CRBC). In the study of the time course of action, an increased ADCC-activity was observed starting at day 10 with a maximum (four-fold augmentation) at day 14 after BCG treatment. The nature of the effector cell was investigated: in normal mice the activity was found in two cell populations, i.e. macrophages and theta-negative (theta-) nylon-adherent spleen cells. A BCG treatment increased the ADCC activity of macrophages of theta- nylon-adherent spleen cells and induced a population of theta- nylon-non-adherent spleen cells. In old mice, the effects of BCG were compared after a weekly long-term (6 months) treatment and after administration of a single dose. It was concluded that ADCC is higher in old mice than in young mice and can be further increased by treatment with a single dose of BCG in contrast with the long-term treatment which impaired this immune reaction.

Published
1980

50. Chimeric peptides: A new approach to enhancing the immunogenicity of peptides with low MHC class I affinity application in antiviral vaccination

Author

Tourdot, S., Oukka, M., Manuguerra, J. C., Vassiliki Magafa, Vergnon, I., Riché, N., Bruley-Rosset, M., Cordopatis, P., and Kosmatopoulos, K.

Subjects
Immunology, Immunology and Allergy
Abstract

Recruitment of the CTL repertoire specific for subdominant epitopes that have a low MHC class I-binding affinity could be the way to achieve an efficient protective immunity against spontaneous tumors and viruses with high mutation rate. However, we have reported recently that subdominant peptides of influenza A Puerto Rico/8/34 (flu PR8) nucleoprotein (NP) with low Db affinity are only partially able to protect mice against lethal influenza infection. This seems to be due to their inability to recruit the specific CTL repertoire, and suggests that subdominant peptides could be used for vaccination only if they become highly immunogenic. In this work, we describe an approach that allows enhancement of the immunogenicity of every low affinity peptide presented by the Db molecule. It consists in producing chimeric peptides composed by amino acids from a high Db affinity peptide (NP366) in positions that interact with the MHC, and amino acids from low Db affinity nonimmunogenic influenza NP-derived peptides (NP17, NP97, NP330, and NP469) in positions that are exposed to the TCR. All chimeric peptides tested exhibited a high Db affinity and efficiently recruited the CTL repertoire specific for the corresponding low Db affinity peptide. Furthermore, vaccination with chimeric peptides that corresponded to subdominant NP17 and NP97 peptides induced a very potent anti-flu PR8 protective immunity.

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