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• W2346261125 abstract "Abstract Efficient processing of target antigens by the ubiquitin-proteasome-system (UPS) is essential for treatment of cancers by T cell therapies. However, immune escape due to altered expression of IFN-γ-inducible components of the antigen presentation machinery and consequent inefficient processing of HLA-dependent tumor epitopes can be one important reason for failure of such therapies. Here, we show that short-term co-culture of Melan-A/MART-1 tumor antigen-expressing melanoma cells with Melan-A/MART-1 26-35 -specific cytotoxic T lymphocytes (CTL) led to resistance against CTL-induced lysis because of impaired Melan-A/MART-1 26-35 epitope processing. Interestingly, deregulation of p97/VCP expression, which is an IFN-γ-independent component of the UPS and part of the ER-dependent protein degradation pathway (ERAD), was found to be essentially involved in the observed immune escape. In support, our data demonstrate that re-expression of p97/VCP in Melan-A/MART-1 26-35 CTL-resistant melanoma cells completely restored immune recognition by Melan-A/MART-1 26-35 CTL. In conclusion, our experiments show that impaired expression of IFN-γ-independent components of the UPS can exert rapid immune evasion of tumor cells and suggest that tumor antigens processed by distinct UPS degradation pathways should be simultaneously targeted in T cell therapies to restrict the likelihood of immune evasion due to impaired antigen processing." @default.
• W2346261125 created "2016-06-24" @default.
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• W2346261125 date "2016-05-04" @default.
• W2346261125 modified "2023-10-14" @default.
• W2346261125 title "Exposure to Melan-A/MART-126-35 tumor epitope specific CD8+T cells reveals immune escape by affecting the ubiquitin-proteasome system (UPS)" @default.
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• W2346261125 doi "https://doi.org/10.1038/srep25208" @default.
• W2346261125 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4855237" @default.
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