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Increased MHC H–2K gene transcription in cultured mouse embryo cells after adenovirus infection

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.

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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

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