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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    International journal of immunogenetics 13 (1986), S. 0 
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Ultraviolet tight (UV)-induced tumours in mice are often highly immunogenic and have unique (individually specific) antigens which cause tumour rejection in normal mice. The molecular nature of these unique ‘rejection’ or ‘transplantation’ antigens is not known. We have recently isolated a syngeneic monoclonal antibody (mAb), CP28, that recognizes a unique tumour-specific antigen on the UV-induced regressor tumour 1591-RE. Further analysis revealed that the antibody-recognized antigen represents a novel major histocompatibility complex (MHC) class I molecule. However, the relationship of this molecule to the unique T cell-recognized antigen that causes tumour rejection remained unresolved. In this study we have explored the relationship of the antibody-defined tumour-specific novel class I molecule to the rejection antigen, that we have previously defined with a cytolytic T cell (CTL) clone (‘anti-A’). Two different lines of evidence suggested a close relationship. First, it was found that random subclones of the 1591-RE tumour expressed different levels of the CP28-defined antigen which correlated with the level of lysis by the anti-A CTL clone. Second, the selection of antigen-loss variants using either the anti-A CTL clone or the mAb CP28 resulted in the simultaneous loss of both the CP28 as well as the ‘A’ antigen. This tight correlation strongly suggests a relationship between the antibody-defined and the T cell-defined antigen. However, the role of the antibody-recognized antigen in causing transplantation rejection still needs to be determined.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The C3H UV-induced fibrosarcoma, 1591, is highly immunogenic and, therefore, is readily rejected when transplanted into immunocompetent syngeneic recipients. Previous analysis of 1591 with tumour-specific or H-2-reactive monoclonal antibodies revealed that this antigenicity might be due to the expression of two novel class I major histocompatibility complex (MHC) antigens. In this report we describe the molecular cloning and initial characterization of three genes which account for all of the unique serological class I reactivities observed on this tumour. These include two distinct, but highly conserved, H-2L-like genes, and a third gene the product of which bears determinants which are characteristic of both the tumour and of class I products of the H-2k haplotype. Moreover, each of these genes contains a polymorphic restriction enzyme fragment which is detected in the class I sequences of 1591 relative to normal C3H tissue. Since the expression of these polymorphic class I sequences is relevant to the immunogenicity of 1591, the mutational events by which these genes were generated may be significant to the immunobiology of this tumour.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Immunology 6 (1988), S. 465-483 
    ISSN: 0732-0582
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The transforming protein E7 of human papilloma virus type 16 can stimulate cytotoxic T lymphocytes (CTL) which can protect experimental animals against growth of E7 expressing tumour cells. In this study we compared CTL responses in mice immunized with either E7 protein in MF59 adjuvant or with recombinant vaccinia virus expressing E7 (Vac-E7). We have chosen H-2d mice because no E7-specific CTL responses have been described in this MHC haplotype. Immunization of these mice with Vac-E7 generated CTL which lysed target cells infected with Vac-E7 or transfected with the E7 gene. CTL from mice immunized with E7 protein in MF59 adjuvant showed specificity for the same target cells. Antibody blocking experiments revealed that both immunization with Vac-E7 and E7 protein stimulated CD8+ effector CTL. The find specificity of CTL induced by the two immunization protocols was similar. A major CTL epitope was mapped to the carboxyl terminal amino acids 48–98 of the E7 protein. Peptide isolation from E7 expressing cells followed by HPLC separation indicated that CTL induced by immunization with protein and Vac-E7 recognized the same HPLC purified peptide fractions. Together, the study suggests that vaccines based on protein can activate CTL with similar fine specificity to CTL induced by vaccines based on recombinant vaccinia virus.
    Type of Medium: Electronic Resource
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