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  • 1
    Digitale Medien
    Digitale Medien
    Ia Antigens as Restriction Molecules in Ir-Gene Controlled T-Cell Proliferation (1981)
    Oxford, UK : Blackwell Publishing Ltd
    Immunological reviews 60 (1981), S. 0 
    Details
    ISSN: 1600-065X
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1600-065X.1981.tb00362.x
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  • 2
    Digitale Medien
    Digitale Medien
    The traditional and a new version of the mouse H–2 complex (1981)
    [s.l.] : Nature Publishing Group
    Nature 291 (1981), S. 455-460 
    Details
    ISSN: 1476-4687
    Quelle: Nature Archives 1869 - 2009
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Notizen: [Auszug] The H–2 complex has traditionally been interpreted as a maze of regions, subregions and loci coding for different traits. The two main theses presented here are, first, that a single H–2 locus is pleiomorphic in that it controls several functions such as allograft rejection, ...
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1038/291455a0
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  • 3
    Digitale Medien
    Digitale Medien
    Induction of lymphokine-activated killer activity in mice by prothymosin α (1994)
    Springer
    Cancer immunology immunotherapy 38 (1994), S. 281-286 
    Details
    ISSN: 1432-0851
    Schlagwort(e): Prothymosin α ; NK and LAK activity ; TNFα ; IL-2
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract We have recently demonstrated that prothymosin α (ProTα) when administered intraperitoneally (i.p.) protects DBA/2 mice against the growth of syngeneic leukemic L1210 cells through the induction of tumoricidal peritoneal cells producing high levels of tumor necrosis factor α (TNFα) [Papanastasiou et al. (1992) Cancer Immunol Immunother 35: 145]. In this report we tested further immunological alterations that may be caused by the administration of ProTα in vivo. We demonstrate that i.p. injections of ProTα enhance natural killer (NK) cell activity and induce lymphokine-activated (LAK) activity in vivo. Thus, splenocytes from ProTα-treated DBA/2 animals exhibited significantly higher cytotoxic activity (up to threefold) against the NK-sensitive YAC cell line and the NK-resistant P815 and L1210 syngeneic tumor cells, as compared to splenocytes from syngeneic control mice. The enhancement of the cytotoxic profile of DBA/2 splenocytes was associated with increased percentages of CD8+ cells, NK cells and activated CD3+ cells. The ProTα-induced effect persisted for 30 days after the end of the ProTα treatment period and returned to normal levels 20 days later. SPlenocytes from non-treated DBA/2 animals generated high NK and LAK activities in response to ProTα in vitro. The ProTα-induced NK an LAK activities reached 84% and 75% respectively of what was obtained with interleukin-2 (IL-2). High concentrations of TNFα and IL-2 were generated in response to ProTα in LAK cultures. These findings suggest that ProTα may provide an overall protective effect against tumor growth in vivo through induction of NK and LAK activities possibly indirectly via the production of IL-2 and TNFα in the spleen, peritoneal cavity and probably other lymphoid organs.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01533521
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  • 4
    Digitale Medien
    Digitale Medien
    Induction of lymphokine-activated killer activity in mice by prothymosin α (1994)
    Springer
    Cancer immunology immunotherapy 38 (1994), S. 281-286 
    Details
    ISSN: 1432-0851
    Schlagwort(e): Key words: Prothymosin α– NK and LAK activity – TNFα– IL-2
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract. We have recently demonstrated that prothymosin α (ProTα) when administered intraperitoneally (i. p.) protects DBA/2 mice against the growth of syngeneic leukemic L1210 cells through the induction of tumoricidal peritoneal cells producing high levels of tumor necrosis factor α (TNFα) [Papanastasiou et al. (1992) Cancer Immunol Immunother 35: 145]. In this report we tested further immunological alterations that may be caused by the administration of ProTα in vivo. We demonstrate that i. p. injections of ProTα enhance natural killer (NK) cell activity and induce lymphokine-activated (LAK) activity in vivo. Thus, splenocytes from ProTα-treated DBA/2 animals exhibited significantly higher cytotoxic activity (up to threefold) against the NK-sensitive YAC cell line and the NK-resistant P815 and L1210 syngeneic tumor cells, as compared to splenocytes from syngeneic control mice. The enhancement of the cytotoxic profile of DBA/2 splenocytes was associated with increased percentages of CD8+ cells, NK cells and activated CD3+ cells. The ProTα-induced effect persisted for 30 days after the end of the ProTα treatment period and returned to normal levels 20 days later. Splenocytes from non-treated DBA/2 animals generated high NK and LAK activities in response to ProTα in vitro. The ProTα-induced NK an LAK activities reached 84% and 75% respectively of what was obtained with interleukin-2 (IL-2). High concentrations of TNFα and IL-2 were generated in response to ProTα in LAK cultures. These findings suggest that ProTα may provide an overall protective effect against tumor growth in vivo through induction of NK and LAK activities possibly indirectly via the production of IL-2 and TNFα in the spleen, peritoneal cavity and probably other lymphoid organs.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01533521
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  • 5
    Digitale Medien
    Digitale Medien
    Increased generation of autologous tumor-reactive lymphocytes by anti-CD3 monoclonal antibody and prothymosin α (1999)
    Springer
    Cancer immunology immunotherapy 48 (1999), S. 71-84 
    Details
    ISSN: 1432-0851
    Schlagwort(e): Key words Anti-CD3 mAb ; Prothymosin α ; Cytotoxicity ; Anticancer activity ; Adoptive immunotherapy
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Anti-CD3 monoclonal antibody (mAb) activates in vitro peripheral blood mononuclear cells (PBMC) to lyse a variety of tumor cell lines in a non-major histocompatibility-complex(MHC)-restricted manner [subsequently referred to as anti-CD3-activated killer (AAK) cytotoxicity]. Prothymosin α (ProTα) is a biological response modifier that exerts its effects primarily on mononuclear cells, especially when these cells' effector functions are impaired. In this study, we report that ProTα enhances the AAK cytotoxicity in PBMC from healthy donors. This effect was more profound with cancer patients' PBMC, which were deficient in their ability to respond with enhanced AAK cytotoxicity upon in vitro stimulation with anti-CD3. Thus, cancer patients' PBMC, activated with a combination of anti-CD3 and ProTα, exhibited increased AAK activity and efficiently lysed both autologous tumor and Daudi targets. The ProTα effect on PBMC was demonstrated to involve stimulation of adhesion molecules (CD2, CD18, CD54, CD49f) and CD25 expression, up-regulation of perforin mRNA transcription, increased numbers of perforin-positive (+) cells and elevated production of interleukin-2 (IL-2), interleukin-1β (IL-1β) and tumor necrosis factor α (TNFα). Moreover, effector CD8+ and CD56+ cells pretreated with anti-CD3 and ProTα contained high cytoplasmic perforin levels and increased expression of IL-1β- and TNFα-specific receptors. The induction of autologous-tumor-reactive CD8+ and CD56+ lymphocytes in anti-CD3-activated PBMC by ProTα provides an alternative protocol aimed at the improvement of clinical results in cellular adoptive immunotherapy of cancer.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/s002620050550
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  • 6
    Digitale Medien
    Digitale Medien
    Synergy between interleukin-2 and prothymosin α for the increased generation of cytotoxic T lymphocytes against autologous human carcinomas (2000)
    Springer
    Cancer immunology immunotherapy 49 (2000), S. 449-458 
    Details
    ISSN: 1432-0851
    Schlagwort(e): Key words Prothymosin-α ; IL-2 ; Autologous tumor ; Cytotoxicity ; CTL
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract  Peripheral blood mononuclear cells (PBMC) from cancer patients were cultured in vitro with irradiated autologous tumor cells isolated from malignant effusions (mixed lymphocyte tumor cultures, MLTC) and low-dose (50 IU/ml) recombinant interleukin-2 (IL-2). The combination of IL-2 and prothymosin α (ProTα) resulted in a greater PBMC-induced response to the autologous tumor than that brought about by IL-2 alone. In particular, ProTα specifically enhanced the CD4+ T-cell-mediated proliferation against the autologous tumor. CD4+ T cells seemed to recognize tumor antigens presented by HLA-DR molecules expressed on the autologous monocytes, since preincubation of the latter with an anti-HLA-DR monoclonal antibody (mAb) abrogated the response. In addition, MLTC set up with IL-2 and ProTα also generated more MHC-class-I-restricted cytotoxic T lymphocytes (CTL) against the autologous tumor than did MLTC set up with IL-2 alone. The MLTC-induced CTL contained high levels of cytoplasmic perforin and their development was strictly dependent on the presence of both autologous CD4+ T cells and monocytes. In the absence of either population there was a strong impairment of both proliferative and cytotoxic responses which was not restored by the presence of ProTα. In contrast, when both cell populations were present, ProTα exerted optimal enhancement of CD4+ T cell proliferation, which was associated with potentiated CTL responses. Our data emphasize the role of ProTα for the enhancement of IL-2-induced CTL responses against autologous tumor cells. Such responses require collaborative interactions between CD4+, CD8+ T cells and monocytes as antigen-presenting cells. Our data are relevant for adoptive immunotherapeutic settings utilizing IL-2 and ProTα-induced autologous-tumor-specific CTL.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/s002620000132
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  • 7
    Digitale Medien
    Digitale Medien
    Promotion of murine antitumour activity by prothymosin α treatment: I. Induction of tumoricidal peritoneal cells producing high levels of tumour necrosis factor α (1992)
    Springer
    Cancer immunology immunotherapy 35 (1992), S. 145-150 
    Details
    ISSN: 1432-0851
    Schlagwort(e): Prothymosin α ; Tumoricidal peritoneal cells ; TNFα
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The effect of prothymosin α (ProTα) on the survival of DBA/2 mice inoculated with syngeneic tumour cells was studied. DBA/2 mice inoculated intraperitoneally (i.p.) with 2×105 syngeneic leukaemic L1210 cells developed ascites within 8–12 days and died 10–14 days later. Treatment with ProTα consistently inhibited the development of ascites in 20% of the treated animals and prolonged the survival of 40%–60% of the animals up to 70 days. The most effective treatment schedule of ProTα was 300 ng/mouse given i.p. at 2-day intervals for 3 weeks followed by a rest period of 7 days, prior to tumour cell inoculation. Peritoneal exudate (PE) cells collected from mice treated with the optimal dose of ProTα produced, in the absence of exogenous stimulus, six- to eightfold higher levels of tumour necrosis factor α (TNFα) than PE cells from control mice. Furthermore these cells exhibited cytotoxic activity against several tumour cell lines including the syngeneic L1210, the TNF-insensitive P815 mastocytoma, the human MOLT-4 lymphoblastic leukaemia, as well as the murine TNF-sensitive L929 fibroblast cell line. Kinetic studies revealed that both production of TNFα and tumoricidal activity peaked 7 days after the last injection of ProTα and were maintained at high levels over a period of 1 month. Injections with 150 ng ProTα slightly improved the survival of mice whereas higher (500 ng and 1000 ng) doses of ProTα and a wide range of thymosin α1 doses remained without any effect. PE cells collected from these mice produced extremely low levels of TNFα and exhibited negligible tumoricidal activity. Our data demonstrate that ProTα has a protective effect in vivo against the growth of adoptively transfered tumour cells and suggest that this effect is, at least in part, mediated by ProTα-activated PE cells. These cells were demonstrated to produce high levels of TNFα in vitro and to exhibit activity against both TNF-sensitive and TNF-resistant cell lines.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01741862
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  • 8
    Digitale Medien
    Digitale Medien
    Induction of tumor-specific T lymphocyte responses in vivo by prothymosin α (1995)
    Springer
    Cancer immunology immunotherapy 40 (1995), S. 410-418 
    Details
    ISSN: 1432-0851
    Schlagwort(e): Prothymosin α ; CTL activity ; Experimental tumors
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract We have recently reported that administration of Pro Tα to DBA/2 mice before the inoculation of syngeneic L1210 leukemic cells prolonged the survival of these animals by (a) inducing tumoricidal peritoneal macrophages, (b) enhancing natural killer (NK) and inducing lymphokine-activated killer (LAK) activities in splenocytes and (c) inducing the production of interleukin-2 and tumor necrosis factor α [Papanastasiou et al. (1992) Cancer Immunol Immunother 35:145; Baxevanis et al. (1994) Cancer Immunol Immunother 38:281]. In this report we demonstrate that Pro T α, when administered simultaneously with L1210 tumor cells, is capable of generating in DBA/2 animals tumorspecific CD8+ cytotoxic T lymphocytes (CTL). The Pro T α-induced CD8+ CTL lysed their syngeneic L1210 targets in a major histocompatibility complex (MHC)-restricted fashion since monoclonal antibodies (mAb) against the H-2Kd allelic product could inhibit the cytotoxic response. Mice receiving only Pro T α developed non-MHC-restricted cytotoxic activity (NK, and LAK activities) whereas those receiving Pro T α and L1210 tumor cells developed both MHC-restricted (CTL) and non-MHC-restricted cytotoxic activities and survived longer. The Pro T α-induced CD8+ CTL activity was regulated by Pro T α-induced L1210-specific syngeneic CD4+ cells. This was shown in two different ways: first, CD8+-cell-mediated cytotoxic responses against L1210 targets were associated with L1210-specific and MHC-restricted proliferative responses of syngeneic CD4+ cells and, second, CD4+ cells from mice that had received both Pro T α and L1210 tumor cells could enhance in vitro the otherwise weak, MHC-restricted and L1210-specific cytotoxicity of syngeneic CD8+ cells from mice that had received only L1210 cells. Our data suggest that Pro T α is capable of inducing nonspecific, as well as tumor-specific CTL responses in vivo. This is of importance since Pro T α may prove to be useful in clinical protocols aimed at cancer immunotherapy.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01525392
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  • 9
    Digitale Medien
    Digitale Medien
    Induction of tumor-specific T lymphocyte responses in vivo by prothymosin α (1995)
    Springer
    Cancer immunology immunotherapy 40 (1995), S. 410-418 
    Details
    ISSN: 1432-0851
    Schlagwort(e): Key words Prothymosin α ; CTL activity ; Experimental tumors
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract  We have recently reported that administration of ProTα to DBA/2 mice before the inoculation of syngeneic L1210 leukemic cells prolonged the survival of these animals by (a) inducing tumoricidal peritoneal macrophages, (b) enhancing natural killer (NK) and inducing lymphokine-activated killer (LAK) activities in splenocytes and (c) inducing the production of interleukin-2 and tumor necrosis factor α [Papanastasiou et al. (1992) Cancer Immunol Immunother 35:145; Baxevanis et al. (1994) Cancer Immunol Immunother 38:281]. In this report we demonstrate that ProTα, when administered simultaneously with L1210 tumor cells, is capable of generating in DBA/2 animals tumor-specific CD8+ cytotoxic T lymphocytes (CTL). The ProTα-induced CD8+ CTL lysed their syngeneic L1210 targets in a major histocompatibility complex(MHC)-restricted fashion since monoclonal antibodies (mAb) against the H-2Kd allelic product could inhibit the cytotoxic response. Mice receiving only ProTα developed non-MHC-restricted cytotoxic activity (NK, and LAK activities) whereas those receiving ProTα and L1210 tumor cells developed both MHC-restricted (CTL) and non-MHC-restricted cytotoxic activities and survived longer. The ProTα-induced CD8+ CTL activity was regulated by ProTα-induced L1210-specific syngeneic CD4+ cells. This was shown in two different ways: first, CD8+-cell-mediated cytotoxic responses against L1210 targets were associated with L1210-specific and MHC-restricted proliferative responses of syngeneic CD4+ cells and, second, CD4+ cells from mice that had received both ProTα and L1210 tumor cells could enhance in vitro the otherwise weak, MHC-restricted and L1210-specific cytotoxicity of syngeneic CD8+ cells from mice that had received only L1210 cells. Our data suggest that ProTα is capable of inducing nonspecific, as well as tumor-specific CTL responses in vivo. This is of importance since ProTα may prove to be useful in clinical protocols aimed at cancer immunotherapy.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01525392
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  • 10
    Digitale Medien
    Digitale Medien
    Selection of H-2 molecules for the context of antigen recognition by T lymphocytes (1981)
    Springer
    Immunogenetics 14 (1981), S. 283-292 
    Details
    ISSN: 1432-1211
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin
    Notizen: Abstract T lymphocytes recognize the synthetic polypeptides GA and GLT and the natural antigen LDHB and are thereby stimulated to proliferate in vitro. Simultaneously with the antigen, T cells recognize class II MHC molecules of the antigen-presenting cell and the T-cell proliferation can therefore be inhibited by the addition of monoclonal antibodies specific for either A (AαA β ) or E (EαF β ) molecules. Antibody blocking of in vitro responses thus provides an opportunity to test the rules governing the selection of class II molecules (A versus E) in the recognition of different antigens. To determine these rules we tested T cells for some 40 strains (classical inbred strains and B10.W lines) carrying H-2 haplotypes derived from wild mice) for their proliferative response to GA, GLT, and LDHB. Strains that responded were then tested in the antibody-blocking assay to determine the class II context of the response. The response to GA occurred always in the context of the A molecule; no single instance was found of the response being channelled through the E molecule. Of the 19 different A molecules (A allomorphs) that could be tested, nine (47 percent) were able to provide the context for GA recognition (and hence conferred responsiveness), while the rest failed to do so (conferred nonresponsiveness). Of the 17 informative cases tested for the response to LDHB, 14 channelled the response through the A molecule, while, in the remaining cases, the cells failed to respond altogether. And again, there was no case where the response was channelled through the E molecule. However, in two instances (of 14) the E molecule provided the context for the stimulation of suppressor T cells, which then suppressed the response of helper T cells occurring in the context of the A molecule. Of the 19 cases tested for the response to GLT, eight channelled the response through the E molecule and two through the A molecule. The two cases of an E → A switch were those in which the strains failed to express cell-surface E molecules as a result of a mutation in one of the E-encoding loci. These data indicate a remarkable but puzzling consistency in the channelling of the response to a given antigen via either A or E molecules. This consistency may be a hint that there is a link between the specificity of antigen (nonself) and MHC (self) recognition by T lymphocytes.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00342197
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