[Molecular analysis of mouse major histocompatibility complex class I gene expression of tumors growing in the brain]

The authors have investigated the regulation of mouse major histocompatibility complex (MHC, H-2) class I gene expression of tumors growing in the brain, by using T-cell lymphoma (Moloney leukemia virus-induced YAC-1 of A/Sn mouse origin) and its cell surface H-2 negative variants, A. H-2- and beta 2m-. FACS analysis showed that low H-2 expressing YAC-1 markedly increased H-2 Kk, Dd and beta-2 microglobulin (beta 2m) induction on the cell surface after intracerebral (i.c.) passage, while there was no change in phenotypical expression of both A. H-2- and beta 2m-. Southern and Northern blot analyses revealed that the enhancement of H-2 class I expression in YAC-1 was due to transcriptional control of H-2 DNA genes. beta 2m- was confirmed to lack beta 2m- gene, causing cell surface H-2 negative expression. Immunoprecipitation method showed that, despite increase in mRNA of the H-2 gene, A. H-2- disclosed no class I H-2 expression because of the incapability of intracellular association of polypeptides between H-2 and beta 2m in the post-translational level. The H-2 class I expression on YAC-1 cells could also be induced by interferon gamma (IFN) in a dose-dependent manner in the range of 1 to 100 U/ml. At 100 U/ml, the H-2 inducing effect, regulated at the transcriptional level, was comparable to that observed after i.c. passage. In contrast, the A. H-2- and beta 2m- remained completely negative after IFN treatment.(ABSTRACT TRUNCATED AT 250 WORDS)