H-2 antigen expression on teratocarcinoma cells passaged in genetically resistant mice is regulated by lymphoid cells. 1981

S Ostrand-Rosenberg, and A Cohn

Previous studies have demonstrated that resistance and susceptibility to the 402AX testicular teratocarcinoma are under genetic control in the mouse. Under normal culture conditions or when passaged in genetically susceptible hosts, the nullipotent 402AX cells do not express H-2 antigens. However, when passaged in genetically resistant animals, the tumor cells become strongly positive for H-2 antigens in the absence of other indications of differentiation. These studies suggested that H-2 antigen modulation on teratocarcinoma cells is mandatory for an effective host cell-mediated immune response against this tumor. The present studies further examine the role of H-2 antigen modulation on teratocarcinoma cells and determine which host cell populations are mediating H-2 modulation on the tumor cells. Reconstitution of lethally irradiated susceptible hosts with resistant bone marrow extends the mean survival time of the host but does not confer complete resistance. Teratocarcinoma cells passaged in such reconstituted hosts do not express H-2 antigens. Two lines of evidence suggest that H-2 antigen modulation is mediated by lymphoid cells: (i) sublethal irradiation of genetically resistant hosts inhibits H-2 antigen modulation on teratocarcinoma cells passaged in vivo and (ii) immunological priming can overcome the loss of H-2 modulation that is normally associated with aging in genetically resistant hosts. Genetically susceptible mice can be fully reconstituted for tumor rejection and H-2 antigen expression on teratocarcinoma cells by reconstitution with genetically resistant bone marrow plus lymphoid cells from tumor-primed resistant hosts. These results: (i) imply the necessity for H-2 antigens on tumor cells for an effective host cell-mediated immune response against the tumor, and (ii) indicate that host lymphoid cells regulate H-2 antigen expression on tumor cells passaged in vivo.

UI MeSH Term Description Entries
D007111 Immunity, Cellular Manifestations of the immune response which are mediated by antigen-sensitized T-lymphocytes via lymphokines or direct cytotoxicity. This takes place in the absence of circulating antibody or where antibody plays a subordinate role. Cell-Mediated Immunity,Cellular Immune Response,Cell Mediated Immunity,Cell-Mediated Immunities,Cellular Immune Responses,Cellular Immunities,Cellular Immunity,Immune Response, Cellular,Immune Responses, Cellular,Immunities, Cell-Mediated,Immunities, Cellular,Immunity, Cell-Mediated,Response, Cellular Immune
D008214 Lymphocytes White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS. Lymphoid Cells,Cell, Lymphoid,Cells, Lymphoid,Lymphocyte,Lymphoid Cell
D008297 Male Males
D008810 Mice, Inbred C57BL One of the first INBRED MOUSE STRAINS to be sequenced. This strain is commonly used as genetic background for transgenic mouse models. Refractory to many tumors, this strain is also preferred model for studying role of genetic variations in development of diseases. Mice, C57BL,Mouse, C57BL,Mouse, Inbred C57BL,C57BL Mice,C57BL Mice, Inbred,C57BL Mouse,C57BL Mouse, Inbred,Inbred C57BL Mice,Inbred C57BL Mouse
D008815 Mice, Inbred Strains Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation. Inbred Mouse Strains,Inbred Strain of Mice,Inbred Strain of Mouse,Inbred Strains of Mice,Mouse, Inbred Strain,Inbred Mouse Strain,Mouse Inbred Strain,Mouse Inbred Strains,Mouse Strain, Inbred,Mouse Strains, Inbred,Strain, Inbred Mouse,Strains, Inbred Mouse
D009374 Neoplasms, Experimental Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms. Experimental Neoplasms,Experimental Neoplasm,Neoplasm, Experimental
D001853 Bone Marrow The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. Marrow,Red Marrow,Yellow Marrow,Marrow, Bone,Marrow, Red,Marrow, Yellow
D006183 H-2 Antigens The major group of transplantation antigens in the mouse. H2 Antigens,Antigens, H-2,Antigens, H2,H 2 Antigens
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D013724 Teratoma A true neoplasm composed of a number of different types of tissue, none of which is native to the area in which it occurs. It is composed of tissues that are derived from three germinal layers, the endoderm, mesoderm, and ectoderm. They are classified histologically as mature (benign) or immature (malignant). (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1642) Dysembryoma,Teratoid Tumor,Teratoma, Cystic,Teratoma, Mature,Teratoma, Benign,Teratoma, Immature,Teratoma, Malignant,Benign Teratoma,Benign Teratomas,Dysembryomas,Immature Teratoma,Immature Teratomas,Malignant Teratoma,Malignant Teratomas,Teratoid Tumors,Teratomas,Teratomas, Benign,Teratomas, Immature,Teratomas, Malignant,Tumor, Teratoid,Tumors, Teratoid

Related Publications

S Ostrand-Rosenberg, and A Cohn
June 1981, Journal of immunology (Baltimore, Md. : 1950),
S Ostrand-Rosenberg, and A Cohn
January 1995, Experimental and clinical immunogenetics,
S Ostrand-Rosenberg, and A Cohn
January 1985, Immunogenetics,
S Ostrand-Rosenberg, and A Cohn
July 1984, Clinical immunology and immunopathology,
S Ostrand-Rosenberg, and A Cohn
December 1988, Biochemical and biophysical research communications,
S Ostrand-Rosenberg, and A Cohn
September 1975, Proceedings of the National Academy of Sciences of the United States of America,
Copied contents to your clipboard!