PMID: 7031669Nov 1, 1981Paper

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

Proceedings of the National Academy of Sciences of the United States of America
S Ostrand-Rosenberg, A L Cohn

Abstract

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 t...Continue Reading

References

Sep 1, 1975·Proceedings of the National Academy of Sciences of the United States of America·J Forman, E S Vitetta
Jan 1, 1977·Immunological Reviews·F Jacob
Nov 1, 1977·Developmental Biology·S Ostrand-RosenbergM A Jewett
Feb 1, 1978·Proceedings of the National Academy of Sciences of the United States of America·E M Eicher, L L Washburn

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Citations

Dec 1, 1984·Cell Differentiation·S Ostrand-RosenbergM Schwartzman
Dec 1, 1984·Cell Differentiation·S GregorováJ Forejt
Oct 1, 1983·Journal of Immunogenetics·P NanniG Prodi

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