HLA class I genes integrated into murine cells are inducible by interferon

AKR leukemias display different amounts of major histocompatibility complex class I antigens on the cell surface. The absence of H-2Kk molecules correlates with the ability of these cell lines to form tumors in vivo as well as to escape lysis by cytotoxic T lymphocytes in vitro. In this report it is shown that the 5' regulatory area of the H-2Kk gene failed to activate transcription in H-2Kk-negative cells. Examination of the proteins interacting with the H-2Kk enhancer in expressing and nonexpressing cells revealed clear differences. In particular, the level of a nuclear protein interacting at position -166 was greatly reduced in the negative cell lines. A transcription factor, known as H2TF1 or KBF1, has been shown previously to interact with this binding site and to be essential for the expression of certain class I genes as well as the expression of beta 2-microglobulin. These results demonstrate that the molecular mechanism of class I gene suppression in malignant tumor cells is at the level of transcription and is most probably modulated by H2TF1/KBFI. In addition, it is shown that the same transcription factor is only present in mouse tissues expressing class I antigens.

supporting

confidence: 72%

A transcription factor interacting with the class I gene enhancer is inactive in tumorigenic cell lines which suppress major histocompatibility complex class I genes.

Henseling¹,

Schmidt²,

Schöler³

et al. 1990

“…strated that the combination of class I enhancer and prorn though interferon is species specific, human class I moter is as efficient as the combination of SV40 enhancer tes, when stably transfected into murine cells, can be and promoter in driving the expression of the cat gene in )erinduced by treatment with mouse interferon (23 (12). The cells were we identified.…”

mentioning

confidence: 89%

A transcriptional enhancer and an interferon-responsive sequence in major histocompatibility complex class I genes.

Vogel¹,

Kress²,

Khoury³

et al. 1986

“…Reports of suppression of MHC class I genes by oncogenes include n-myc in neuroblastoma cell lines (3), v-src in transformed human fibroblasts (10), and c-myc in human melanoma cell lines (37). Since MHC class I antigen expression is enhanced in a wide variety of cells by all three types of interferons (alpha, beta, and gamma) (8,23,30,40). Other agents which can enhance MHC class I gene expression include retinoic acid in F9 teratocarcinoma cells (35) and sodium butyrate in K562 cells (34).…”

mentioning

confidence: 99%

“…The cells were incubated in the conditioned medium for 24 h, the medium was removed, the cells were washed with PBS, and 104 PFU of vesicular stomatitis virus in DME without serum was added to each well. Cells were scored for lysis between 30 and 48 h after addition of the virus. The cells were stained with 0.05% amido blue black in 9% acetic acid with 0.1 M sodium acetate and fixed with 10% formaldehyde and 9% acetic acid with 0.1 M sodium acetate.…”

mentioning

confidence: 99%

Autocrine induction of major histocompatibility complex class I antigen expression results from induction of beta interferon in oncogene-transformed BALB/c-3T3 cells.

Offermann¹,

Faller²

1989