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- Title
Analysis of the MHC Class I Antigen Presentation Machinery in Human Embryonal Carcinomas: Evidence for Deficiencies in TAP, LMP and MHC Class I Expression and their Upregulation by IFN-γ.
- Authors
Seliger, B.; Dunn, T.; Schwenzer, A.; Casper, J.; Huber, C.; Schmoll, H. J.
- Abstract
The expression of the major histocompatibility complex (MHC) class I antigens is suppressed in early post-implantation embryonic cells as well as in embryonal carcinoma (EC) cells, but could be upregulated by treatment with interferon (IFN)-γ or relinoic acid. In a number of human and murine tumours, defects in the expression of the different components of the MHC class I antigen processing machinery, such as the proteasomal subunits LMP-2 and LMP-7 and the peptide transporters TAP-1 and TAP-2, account for impaired MHC class I surface expression. Here, we analysed the constitutive and IFN-γ regulated mRNA and protein expression of the LMP, TAP and MHC class I molecules in the human EC line 577LM. In comparison to lymphoblastoid control cells, poor constitutive mRNA and protein expression of LMP-7, TAP-1, HLA class I, and β2-microglobulin, but not of TAP-2 and LMP-2, was detected in 577LM cells. The lack of MHC class I surface expression on 577LM cells could not be enhanced either by culturing cells at low temperature or by their incubation with exogenous MHC class I specific binding peptides: thus, the defective MHC class I surface expression was not only caused by impaired generation and processing of antigenic peptides. IFN-γ treatment of 577LM resulted in a significant increase of MHC class I surface expression which was preceded by an upregulation of TAP, LMP and MHC class I transcripts as well as of TAP-1 and TAP-2. but not of LMP-2 and LMP-7, protein expression. These data suggest that human EC cell lines show a stable expression of a MHC class I low/deficient phenotype. The deficiencies associated with this phenotype involve different levels of the MHC class I restricted antigen presentation machinery and could be modified by treatment with IFN-γ.
- Subjects
ANTIGENS; CANCER; CELLS; INTERFERONS; MESSENGER RNA
- Publication
Scandinavian Journal of Immunology, 1997, Vol 46, Issue 6, p625
- ISSN
0300-9475
- Publication type
Article
- DOI
10.1046/j.1365-3083.1997.d01-176.x