Proto-oncogene PML controls genes devoted to MHC class I antigen presentation

Pan Zheng, Yong Guo, Qingtian Niu, David E. Levy, Jacqueline A. Dyck, Shengli Lu, Lori A. Sheiman and Yang Liu ()
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Pan Zheng: Ohio State University Medical Center
Yong Guo: New York University Medical Center
Qingtian Niu: New York University Medical Center
David E. Levy: New York University Medical Center
Jacqueline A. Dyck: University of California at San Diego
Shengli Lu: New York University Medical Center
Lori A. Sheiman: New York University Medical Center
Yang Liu: Ohio State University Medical Center

Nature, 1998, vol. 396, issue 6709, 373-376

Abstract: Abstract Fragments of foreign antigens associated with class I molecules of the major histocompatibility complex (MHC) are presented at the cell surface to elicit an immune response. This presentation requires the coordinated expression of several genes contained in the MHC1,2,3,4,5, including those encoding the MHC class I heavy chain, the proteins LMP-2 and LMP-7, which are involved in the proteasomal degradation of cytosolic antigens into peptide fragments that are destined for association with MHC class I molecules, and TAP-1 and TAP-2, which transport these fragments across the membrane of the endoplasmic reticulum at the start of their journey to the cell surface. In many virus-transformed cell lines6,7 and spontaneous tumours8,9,10, these genes are simultaneously repressed. However, the key factor(s) that are essential for their expression and repression have not been identified. Here we report that the proto-oncogene product PML induces expression of LMP-2, LMP-7, TAP-1 and TAP-2 in an MHC-class I-negative, recurrent tumour, leading to the re-expression of cell-surface MHC in tumours and to rejection of the tumours. PML also regulates MHC expression in untransformed fibroblasts. We conclude that malfunction of PML may enable a tumour to evade the immune defence of its host.

Date: 1998
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DOI: 10.1038/24628

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