Effect of mouse interferon on the expression of a porcine major histocompatibility gene introduced into mouse L cells.

Mouse L cells transformed with a swine genomic clone, which encodes a major histocompatibility (MHC) antigen (SLAd), stably express SLAd on their surface. Mouse interferon (IFN) markedly enhances the expression of the heterologous SLAd as well as endogenous H-2k antigens in two independent transformants, as measured by flow microfluorometry. The expression of an unrelated surface antigen, gp70, is not affected. The increased expression of SLAd antigens is the result of an increased pool of SLA mRNA in IFN-treated cells. In vitro nuclear transcription experiments suggest that this increased accumulation of SLA mRNA results largely from an enhanced transcription of the heterologous SLA gene. The effect of IFN is not restricted to the MHC coding sequences; the transcription of two DNA sequence elements flanking the SLA gene, which are constitutively expressed in one L cell transformant, is also enhanced by IFN. In contrast, in another transformant these same flanking sequences are not transcribed and do not respond to IFN. The results suggest that IFN enhances the transcription of MHC coding and the flanking sequences that are expressed in its absence, but it does not appear to induce do novo transcription of the silent flanking genes examined.