Animals bearing malignant grafts reject normal grafts that express through gene transfer the same antigen

Breaking the state of immunological unresponsiveness of tumor-bearing individuals to cancer is a prerequisite for active or passive tumor-specific immunotherapy. To study this problem the immunogenic MHC class I antigen, K216 was transfected into a progressor tumor. The transfected tumors were regul...

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Published inThe Journal of experimental medicine Vol. 171; no. 4; pp. 1205 - 1220
Main Authors PERDRIZET, G. A, ROSS, S. R, STAUSS, H. J, SINGH, S, KOEPPEN, H, SCHREIBER, H
Format Journal Article
LanguageEnglish
Published New York, NY Rockefeller University Press 01.04.1990
The Rockefeller University Press
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Abstract Breaking the state of immunological unresponsiveness of tumor-bearing individuals to cancer is a prerequisite for active or passive tumor-specific immunotherapy. To study this problem the immunogenic MHC class I antigen, K216 was transfected into a progressor tumor. The transfected tumors were regularly rejected by normal mice but grew progressively in mice bearing nontransfected tumors. In addition, transgenic mice were derived to obtain normal cells and tissues expressing the same K216 gene product. Normal mice rejected K216-positive normal or malignant tissue grafts and generated K216-specific CTL in vitro and in vivo in response to these challenges. In contrast, mice bearing nontransfected tumors, though rejecting K216-positive nonmalignant tissue grafts, did not reject K216-positive tumors nor generate K216-specific CTL in response to K216-positive tumor cells. Mice bearing K216-positive tumors also rejected the nonmalignant K216-positive tissue grafts, but this in vivo response failed to lead to rejection of the simultaneously present tumor graft expressing the same antigen; in fact, immunity had no measurable effect whatsoever on tumor size or incidence and caused no selection for antigen loss variants. Taken together, the present findings suggest that transfer of expression of a target antigen into nonmalignant cells provides a way for obtaining effective stimulation of antigen-specific CTL in tumor-bearing mice, but that additional manipulations will be required to cause immunological rejection of established tumors.
AbstractList Breaking the state of immunological unresponsiveness of tumor-bearing individuals to cancer is a prerequisite for active or passive tumor-specific immunotherapy. To study this problem the immunogenic MHC class I antigen, K216 was transfected into a progressor tumor. The transfected tumors were regularly rejected by normal mice but grew progressively in mice bearing nontransfected tumors. In addition, transgenic mice were derived to obtain normal cells and tissues expressing the same K216 gene product. Normal mice rejected K216-positive normal or malignant tissue grafts and generated K216-specific CTL in vitro and in vivo in response to these challenges. In contrast, mice bearing nontransfected tumors, though rejecting K216-positive nonmalignant tissue grafts, did not reject K216-positive tumors nor generate K216-specific CTL in response to K216-positive tumor cells. Mice bearing K216-positive tumors also rejected the nonmalignant K216-positive tissue grafts, but this in vivo response failed to lead to rejection of the simultaneously present tumor graft expressing the same antigen; in fact, immunity had no measurable effect whatsoever on tumor size or incidence and caused no selection for antigen loss variants. Taken together, the present findings suggest that transfer of expression of a target antigen into nonmalignant cells provides a way for obtaining effective stimulation of antigen-specific CTL in tumor-bearing mice, but that additional manipulations will be required to cause immunological rejection of established tumors.
Breaking the state of immunological unresponsiveness of tumor-bearing individuals to cancer is a prerequisite for active or passive tumor-specific immunotherapy. To study this problem the immunogenic MHC class I antigen, K super(216) was transfected into a progressor tumor. The transfected tumors were regularly rejected by normal mice but grew progressively in mice bearing nontransfected tumors. Taken together, the present findings suggest that transfer of expression of a target antigen into nonmalignant cells provides a way for obtaining effective stimulation of antigen-specific CTL in tumor-bearing mice, but that additional manipulations will be required to cause immunological rejection of established tumors.
Author PERDRIZET, G. A
KOEPPEN, H
SINGH, S
SCHREIBER, H
STAUSS, H. J
ROSS, S. R
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Issue 4
Keywords Flow cytometry
Immune response
Rodentia
Transgenic animal
Cytotoxicity
Host
Rejection
Vertebrata
Mammalia
Transfection
Mouse
Graft
Tumor
Class I histocompatibility antigen
Tumor cell
Language English
License CC BY 4.0
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Snippet Breaking the state of immunological unresponsiveness of tumor-bearing individuals to cancer is a prerequisite for active or passive tumor-specific...
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StartPage 1205
SubjectTerms Animals
Biological and medical sciences
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Graft Rejection - genetics
Graft Rejection - immunology
Histocompatibility Antigens Class I - genetics
Major Histocompatibility Complex
Mice
Mice, Inbred BALB C
Mice, Inbred C3H
Mice, Inbred C57BL
Mice, Transgenic
Neoplasm Transplantation
Skin Neoplasms - genetics
Skin Neoplasms - immunology
Skin Transplantation - immunology
Tissue, organ and graft immunology
Transfection
Title Animals bearing malignant grafts reject normal grafts that express through gene transfer the same antigen
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Volume 171
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