| http://purl.uniprot.org/citations/25875653 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25875653 | http://www.w3.org/2000/01/rdf-schema#comment | "While the immune system has the capacity to recognize and destroy melanoma, tolerance mechanisms often hinder the development of effective anti-tumor immune responses. Since many melanoma antigens are self proteins expressed in normal melanocytes, self antigen exposure before tumor development can negatively impact the function of T cells specific for these self/tumor antigens. However, the contribution of self tolerance to anti-melanoma T cell dysfunction remains largely unexplored. We have previously described a TCR transgenic (Tg) mouse model in which T cells specific for the self/melanoma antigen, tyrosinase-related protein 1 (TRP1), develop in the presence of endogenous TRP1 expression (Ag+) and diminished antigen presentation due to the absence of gamma-interferon-inducible lysosomal thiol reductase (GILT-/-). We show that TRP1-specific T cells from these Ag+GILT-/-Tg mice do not protect from melanoma tumor growth, fail to induce autoimmune vitiligo, and undergo diminished proliferation compared to T cells from Ag-GILT+/+Tg mice. Despite an increased frequency of TRP1-specific Treg cells in Ag+GILT-/-Tg mice compared to Ag-GILT+/+Tg animals, Treg cell depletion only partially rescues the proliferative capacity of T cells from TRP1-expressing mice, suggesting the involvement of additional suppressive mechanisms. An increased percentage of melanoma-specific T cells from Ag+GILT-/-Tg animals express PD-1, an inhibitory receptor associated with the maintenance of T cell exhaustion. Antibody blockade of PD-1 partially improves the ability of TRP1-specific T cells from Ag+GILT-/-Tg mice to produce IL-2. These findings demonstrate that melanoma-specific T cells exposed to a self/melanoma antigen in healthy tissue develop an exhaustion-like phenotype characterized by PD-1-mediated immunosuppression prior to encounter with tumor."xsd:string |
| http://purl.uniprot.org/citations/25875653 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0123332"xsd:string |
| http://purl.uniprot.org/citations/25875653 | http://purl.uniprot.org/core/author | "Hastings K.T."xsd:string |
| http://purl.uniprot.org/citations/25875653 | http://purl.uniprot.org/core/author | "Rausch M.P."xsd:string |
| http://purl.uniprot.org/citations/25875653 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/25875653 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
| http://purl.uniprot.org/citations/25875653 | http://purl.uniprot.org/core/pages | "e0123332"xsd:string |
| http://purl.uniprot.org/citations/25875653 | http://purl.uniprot.org/core/title | "An exhaustion-like phenotype constrains the activity of CD4+ T cells specific for a self and melanoma antigen."xsd:string |
| http://purl.uniprot.org/citations/25875653 | http://purl.uniprot.org/core/volume | "10"xsd:string |
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