Abstract
The class I major histocompatibility complex (MHC) antigens are highly polymorphic1 cell-surface proteins2 whose expression is essential for the cellular immune response against virus-infected, abnormal and foreign cells3,4. Transformation of primary rat cell cultures by the oncogenic adenovirus 12 (Ad 12) results in suppression of the transplantation antigens5, thus enabling the transformed cells to escape the immune response and efficiently form tumours in vivo6. In contrast, transformation of the same cells with the non-oncogenic adenovirus 5 (Ad5) does not suppress the transplantation antigens5 and, consequently, they elicit an effective (MHC-restricted) immune response6. Here, however, we show that infection of mouse embryo cells with both viruses initially increases the level of transcripts from the H–2Kb transplantation antigen gene. Both the adenovirus E1a (12S RNA) and E1b genes are required for activation of the H–2K gene and measurement of the relative rate of transcription indicates that the increase in the level of H–2K messenger RNA following infection is at least in part due to a gene-specific transcriptional activation. The newly transcribed H–2Kb mRNA is then properly transported to the cytoplasm.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 51 print issues and online access
$199.00 per year
only $3.90 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
Similar content being viewed by others
References
Klein, J. Science 203, 516–521 (1979).
Ploegh, H. L., Orr, H. T. & Strominger, J. L. Cell 24, 287–299 (1981).
Steinmetz, M., Winoto, A., Minard, K. & Hood, L. Cell 28, 489–498 (1982).
Klein, J. Biology of the Mouse Histocompatibility-2 Complex (Springer, Berlin, 1975).
Schrier, P. I., Bernards, R., Vaessen, R. T. M. J., Houweling, A. & van der Eb, A. J. Nature 305, 771–775 (1983).
Bernards, R. et al. Nature 305, 776–779 (1983).
Rosenthal, A., Wright, S., Cedar, H., Flavell, R. & Grosveld, F. Nature 310, 415–418 (1984).
Shenk, T., Jones, N., Colby, W. & Fowlkes, D. Cold Spring Harb. Symp. quant. Biol. 44, 367–375 (1980).
Jones, N. & Shenk, T. Cell 17, 683–689 (1979).
Gallimore, P. et al. Cancer Cells Vol. 2 (eds Vande Woude, G. F. et al.) 519–526 (Cold Spring Harbor Laboratory, New York, 1984).
Berk, A. J., Lee, F., Harrison, T., Williams, J. & Sharp, P. A. Cell 17, 935–944 (1979).
Jones, N. & Shenk, T. Proc. natn. Acad. Sci. U.S.A. 76, 3665–3669 (1979).
Nevins, J. R. Cell 26, 213–220 (1981).
Richardson, W. D. & Westphal, H. Current Topics Microbiol. Immun. 109, 147–165 (1983).
Green, M. R., Treisman, R. & Maniatis, T. Cell 35, 137–148 (1983).
Imperiale, M. J., Feldman, L. T. & Nevins, J. R. Cell 35, 127–136 (1983).
Svensson, C & Akusjarvi, G. EMBO J. 3, 789–794 (1984).
Gaynor, R. B., Hillman, D. & Berk, A. J. Proc. natn. Acad. Sci. U.S.A. 81, 1193–1197 (1984).
Curtois, G. & Berk, A. EMBO J. 3, 1145–1149 (1984).
Nevins, J. R. Cell 29, 913–919 (1982).
Katze, M. G., Persson, H., Johasson, B.-M. & Philipson, L. J. Virol. 46, 50–59 (1983).
Katze, M. G., Persson, H. & Philipson, L. Molec. cell. Biol. 1, 807–813 (1981).
Pääbo, S. et al. Prog. Allergy 36, 114–134 (1985).
Sarnow, P., Ho, Y. S., Williams, J. & Levine, A. J. Cell 28, 387–394 (1982).
Brickell, P. M., Latchman, D. S., Murphy, D., Willison, K. & Rigby, P. W. J. Nature 306, 756–760 (1983).
Raška, K. & Gallimore, P. H. Virology 123, 8–18 (1982).
Mellow, G. H., Föhring, B., Dougherty, J., Gallimore, P. H. & Raška, K. Virology 134, 460–465 (1984).
Lewis, A. M. & Cook, J. L. Science 227, 15–20 (1985).
Hui, K., Grosveld, F. & Festenstein, H. Nature 311, 750–752 (1984).
Berk, A. J. & Sharp, P. A. Cell 12, 721–732 (1977).
Weaver, R. F. & Weissmann, C. Nucleic Acids Res 6, 1175–1193 (1979).
Groudine, M. & Casimir, C. Nucleic Acids Res. 12, 1427–1446 (1984).
Kafatos, F. C., Jones, C. W. & Efstratiadis, A. Nucleic Acids Res. 7, 1541–1552 (1979).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Rosenthal, A., Wright, S., Quade, K. et al. Increased MHC H–2K gene transcription in cultured mouse embryo cells after adenovirus infection. Nature 315, 579–581 (1985). https://doi.org/10.1038/315579a0
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1038/315579a0
This article is cited by
-
Human cytomegalovirus in the pancreas of patients with type 2 diabetes: Is there a relation to clinical features, mRNA and protein expression of insulin, somatostatin, and MHC class II?
Virchows Archiv A Pathological Anatomy and Histopathology (1992)
-
The class I major histocompatibility antigen gene activated in a line of SV40-transformed mouse cells is H–2Dd, not Qa/Tla
Nature (1985)
Comments
By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.