An active T-cell-independent mechanism enhances MHC class I transcription and expression on a mouse T-cell lymphoma in vivo.

The present study focuses on the mechanism underlying changes in H-2 cell surface antigen expression after passage of the in vitro grown YAC-1 lymphoma as an ascites tumor. The increase in cell-surface expression correlated with elevated levels of class I transcripts as revealed by Northern blots. The enhanced H-2 expression was also seen with a cloned YAC-1 line, and not until 2 weeks after in vitro explantation had levels of H-2 decreased to those on the in vitro established YAC-1. Arguing for the necessity of a mature functioning immune system, suckling mice were unable to increase H-2 expression on inoculated lymphoma cells. Also pretreatment with cyclophosphamide or irradiation abolished the capacity of adult mice to increase cell surface H-2 on YAC-1 cells. A functioning T-cell system was not required for H-2 enhancement to occur since athymic nude mice were fully competent. The possible significance of an active T-cell-independent host mechanism which enhances tumor H-2 expression at the transcriptional level is discussed.