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  • 1
    Online Resource
    Online Resource
    Elsevier BV ; 1990
    In:  Cellular Immunology Vol. 126, No. 1 ( 1990-03), p. 80-90
    In: Cellular Immunology, Elsevier BV, Vol. 126, No. 1 ( 1990-03), p. 80-90
    Type of Medium: Online Resource
    ISSN: 0008-8749
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1990
    detail.hit.zdb_id: 80094-6
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  • 2
    In: The Journal of Infectious Diseases, Oxford University Press (OUP), Vol. 179, No. 3 ( 1999-03), p. 558-566
    Type of Medium: Online Resource
    ISSN: 0022-1899 , 1537-6613
    URL: Issue
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 1999
    detail.hit.zdb_id: 3019-3
    detail.hit.zdb_id: 1473843-0
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  • 3
    Online Resource
    Online Resource
    BMJ ; 2015
    In:  Journal for ImmunoTherapy of Cancer Vol. 3, No. S2 ( 2015-12)
    In: Journal for ImmunoTherapy of Cancer, BMJ, Vol. 3, No. S2 ( 2015-12)
    Type of Medium: Online Resource
    ISSN: 2051-1426
    Language: English
    Publisher: BMJ
    Publication Date: 2015
    detail.hit.zdb_id: 2719863-7
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  • 4
    Online Resource
    Online Resource
    Wiley ; 1993
    In:  European Journal of Immunology Vol. 23, No. 10 ( 1993-10), p. 2592-2596
    In: European Journal of Immunology, Wiley, Vol. 23, No. 10 ( 1993-10), p. 2592-2596
    Abstract: In attempt to increase the induction of peptide‐specific cytolytic T cells (CTL) we investigated the effect of the Newcastle disease virus (NDV) hemagglutinin‐neuraminidase (HN) gene product on the activation of peptide‐specific CTL. Spleen cells of CH3 mice immunized against the influenza nucleoprotein peptide 50–63 (NP 50–63) were restimulated in vitro (i) with peptide‐pulsed syngeneic fibroblast cells (Ltk − ) as antigen‐presenting cells, which were in addition (ii) infected with NDV or (iii) stably transfected with the HN cDN A of NDV. A greater than sixfold increase in peptide‐specific CTL responses was observed in cultures restimulated with peptide‐pulsed Ltk − cells which co‐expressed viral hemagglutinin due to either infection or transfection. A similar augmentation was seen in CTL responses against other types of antigen (major histocompatibility complex alloantigens, minor histocompatibility antigens or tumor antigens) when suboptimal cultures were stimulated with the respective antigen‐presenting cells modified by NDV infection. These findings suggest that NDV or viral HN expressed on antigen‐presenting cells or tumor cells can exert a T cell co‐stimulatory function.
    Type of Medium: Online Resource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 1993
    detail.hit.zdb_id: 120108-6
    detail.hit.zdb_id: 1491907-2
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  • 5
    Online Resource
    Online Resource
    Wiley ; 1994
    In:  International Journal of Cancer Vol. 58, No. 2 ( 1994-07-15), p. 275-284
    In: International Journal of Cancer, Wiley, Vol. 58, No. 2 ( 1994-07-15), p. 275-284
    Abstract: To study metastasis at the single‐cell level we transduced highly metastatic ESb lymphoma cells with a retroviral expression vector containing the lacZ (bacterial β‐galactosidase) gene. This allowed single ESb‐lacZ tumor cells to be detected in infiltrated target organs by means of X‐Gal staining. Despite expression of the lacZ gene, the tumor cells were still tumorigenic, highly metastatic, unchanged in phenotype and therefore comparable to parental ESb cells. After spontaneous metastasis, whole‐organ staining revealed metastatic foci at the surface of the liver. In histological liver sections, metastatic clusters and single dispersed tumor cells could be detected. In contrast to whole‐organ staining, histological examination revealed scattered distribution of tumor cells throughout the organ, which was not evident with parental ESb cells. In addition, clusters with diffuse or dense (focal) appearance were found, in correlation with the whole‐organ staining. Expression of the foreign lacZ gene allowed the metastatic spread of tumor cells to liver and spleen to be quantified approximately by FACS analysis. Furthermore, it was shown that the newly expressed β‐gal was expressed not only intercellularly but also at the cell surface. There it could be recognized by MAbs and cytotoxic T‐cells (CTL). β‐gal did not affect CTL recognition of the ESb tumor‐associated antigen. In conclusion, lacZ could be used as a genetic marker for a highly metastatic lymphoma, to define scattered metastatic spread in the liver at the single‐cell level and to quantify the tumor load by FACS analysis.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 1994
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 6
    In: Immunology & Cell Biology, Wiley, Vol. 71, No. 4 ( 1993-08), p. 311-326
    Abstract: This study demonstrates that a syngeneic specific cytotoxic T lymphocyte (CTL) response to a class I major histocompatibility complex (MHC) positive tumour requires dual processing and recognition of tumour antigens. One type of antigen is processed and expressed in association with class I MHC at the surface of intact tumour cells. It is recognized by CD8 α,β TCR CTL in vitro and by protective immune T cells in vivo and thus functions as a tumour‐associated transplantation antigen (TATA). The other type of antigen is processed and expressed by distinct host APC in association with class II MHC. This is recognized by immune CD4 T cells which function as essential helper cells in the generation of the CD8 CTL response. These conclusions are supported by cell depletion and reconstitution experiments as well as by blocking experiments with monoclonal antibodies using the highly metastatic class II negative murine lymphoma ESb as a model system. The existence of two types of cognate T cell responses in a syngeneic anti‐tumour response was directly proved by the establishment of two types of tumour specific T cell lines which required as co‐stimulator either MHC class II positive APC or IL‐2. In suboptimal mixed lymphocyte tumour cell cultures either of these co‐stimulator functions was found to be limiting the overall anti‐tumour CTL response. The generation of the tumour specific CTL response could be blocked by monoclonal antibodies against all the molecules involved in the cognate interactions (i.e. class I MHC, CD8, class II MHC, CD4 and TCR) but not by anti‐CD2 or anti‐IgG. The strict requirement for helper cells and APC could be bypassed by the addition of recombinant IL‐2 but optimal triggering of CD8 CTL‐precursor required viable tumour stimulator cells. This well characterized in vitro assay may be useful (i) for monitoring the immune status of CD4 and CD8 immune T cells separately, for instance of tumour bearing and/or treated animals and (ii) for the development and testing of potent tumour cell vaccines with T cell stimulatory and/or co‐stimulatory activities.
    Type of Medium: Online Resource
    ISSN: 0818-9641 , 1440-1711
    Language: English
    Publisher: Wiley
    Publication Date: 1993
    detail.hit.zdb_id: 2011707-3
    detail.hit.zdb_id: 284057-1
    SSG: 12
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  • 7
    In: Retrovirology, Springer Science and Business Media LLC, Vol. 9, No. S1 ( 2012-12)
    Type of Medium: Online Resource
    ISSN: 1742-4690
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2012
    detail.hit.zdb_id: 2142602-8
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Wiley ; 1988
    In:  European Journal of Immunology Vol. 18, No. 8 ( 1988-08), p. 1159-1166
    In: European Journal of Immunology, Wiley, Vol. 18, No. 8 ( 1988-08), p. 1159-1166
    Abstract: The present study elucidates the mechanism whereby viral xenogenization of highly metastatic ESb lymphoid tumor cells increases tumor immunogenicity and syngeneic tumor‐specific T cell responses in comparison to nonmodified tumor cells. It was found that the frequency of cytotoxic T lymphocytes specific for the ESb tumor‐associated transplantation antigen (TATA) and the cytotoxic anti‐tumor activity in bulk cultures of immune spleen cells were significantly increased (by factor 3 and 25, respectively) when using virus‐modified tumor cells. An amplified response was observed both in vivo and in vitro which might explain the demonstrated effectiveness of this approach for postoperative immunotherapy of ESb metastases. For the stimulation of tumor‐specific cytolytic T lymphocytes (CTL) the ESb tumor cells which are highly metastatic were infected with an avirulent strain of the paramyxovirus Newcastle Disease Virus (NDV). Infection of ESb cells with low amounts of NDV was sufficient to lead to an increase in cytolytic activity of tumor‐specific CTL after sensitization in vivo and restimulation in vitro. In a sensitive limiting dilution mixed leukocyte‐tumor cell microculture system the direct effect of viral modification on the frequency and specificity of CTL was investigated. The number of ESb‐specific CTL per spleen could be raised from about 3300 (without modification) to 9100 by both in vivo and in vitro application of ESb‐NDV. One appliction of ESb‐NDV ( in vivo or in vitro ) increased the number of CTL to 4900 and 4600, respectively. In split‐type experiments it could be shown at the clonal level that viral modification did not alter the specificity of ESb‐specific CTL. No CTL clones directed against viral antigens or new antigenic determinants were detected. The results indicate that in this system the effect of viral xenogenization is not due to recognition of additional xenoor neoantigens. NDV modification instead led to a selective augmentation of the TATA‐specific CTL response. In this respect it is remarkable since other methods to increase ESb tumor immunogenicity such as mutagenization or co‐expression of minor H antigens were shown before to activate additional CTL clones without affecting the TATA‐specific CTL response.
    Type of Medium: Online Resource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 1988
    detail.hit.zdb_id: 120108-6
    detail.hit.zdb_id: 1491907-2
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  • 9
    In: European Journal of Immunology, Wiley, Vol. 19, No. 2 ( 1989-02), p. 341-346
    Abstract: Previously we described a monoclonal antibody (mAb 12–15) that reacted with murine Fc receptor proteins (betal, beta2 and alpha) and an undefined molecule of 37 kDa (beta3) on certain types of cells. Here we present serological and biochemical evidence that the beta3 chain is expressed on mouse thymocytes and that it is identical to the CD2 antigen. By immunofluorescence staining and cytofluorographic analysis 〉 95% of thymocytes were positive. Brightly staining cells coincided with cortison‐resistant thymocytes suggesting that mature thymocytes expressed higher levels of the antigen. Biosynthetic labeling of DBA/2 thymocytes with [ 35 S]methionine showed that the size of the CD2 precursor molecule was 43 kDa which was processed to approximately 55–65 kDa in the mature molecule. mAb 12–15 was also reactive with the tunicamycin‐treated form of the CD2 antigen suggesting that the cross‐reactive epitope was of protein nature. Comparison of different mouse strains indicated that two molecular forms of CD2 exist. On BALB/c thymocytes, the relative mass of the native molecule was approximately 60–70 kDa (CD2.1) and slightly larger than in DBA/2 (CD2.2). Following endoglycosidase F treatment both proteins still showed a slight difference in electrophoretic mobility. Several inbred mouse strains were analyzed for expression of CD2 forms. When mAb 12–15 was used in cyotoxic T lymphocyte inhibition experiments using specific CTL and tumor target cells it was found that the antibody could specifically inhibit CTL‐mediated lysis presumably by interfering with CD2 function.
    Type of Medium: Online Resource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 1989
    detail.hit.zdb_id: 120108-6
    detail.hit.zdb_id: 1491907-2
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  • 10
    Online Resource
    Online Resource
    Wiley ; 1987
    In:  European Journal of Immunology Vol. 17, No. 12 ( 1987-01), p. 1863-1866
    In: European Journal of Immunology, Wiley, Vol. 17, No. 12 ( 1987-01), p. 1863-1866
    Abstract: A role of CD4 + T helper cells in induction of tumor transplant rejection leading to complete regression of a highly metastatic DBA/2 mouse lymphoma was analyzed. Using an anti‐CD4 monoclonal antibody (GK1.5) which eliminates T helper cells in vivo and in vitro , we found that CD4 + cells are required for tumor resistance in syngeneic DBA/2 mice or allogeneic but major histocompatibility complex‐identical B10.D2 mice. In contrast, in allogeneic C57BL/6 mice tumor rejection was independent of CD4 + cells. An analogous requirement for immune CD4 + cells for in vitro induction of CD8 + tumor‐specific cytotoxic T cells was found in these respective strains. The requirement for immune CD4 + cells in vitro could be replaced by recombinant interleukin 2. These results demonstrate a role of CD4 + regulatory T cells and T‐T cell cooperation in the induction of anti‐tumor immunity and tumor rejection, and point to possible therapeutic interventions in the afferent phase of anti‐tumor immune responses.
    Type of Medium: Online Resource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 1987
    detail.hit.zdb_id: 120108-6
    detail.hit.zdb_id: 1491907-2
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