Identification of Special AT-Rich Sequence Binding Protein 1 as a Novel Tumor Antigen Recognized by CD8 T Cells: Implication for Cancer ImmunotherapyReport as inadecuate




Identification of Special AT-Rich Sequence Binding Protein 1 as a Novel Tumor Antigen Recognized by CD8 T Cells: Implication for Cancer Immunotherapy - Download this document for free, or read online. Document in PDF available to download.

Background

A large number of human tumor-associated antigens that are recognized by CD8+ T cells in a human leukocyte antigen class I HLA-I-restricted fashion have been identified. Special AT-rich sequence binding protein 1 SATB1 is highly expressed in many types of human cancers as part of their neoplastic phenotype, and up-regulation of SATB1 expression is essential for tumor survival and metastasis, thus this protein may serve as a rational target for cancer vaccines.

Methodology-Principal Findings

Twelve SATB1-derived peptides were predicted by an immuno-informatics approach based on the HLA-A*02 binding motif. These peptides were examined for their ability to induce peptide-specific T cell responses in peripheral blood mononuclear cells PBMCs obtained from HLA-A*02+ healthy donors and-or HLA-A*02+ cancer patients. The recognition of HLA-A*02+ SATB1-expressing cancer cells was also tested. Among the twelve SATB1-derived peptides, SATB1565–574 frequently induced peptide-specific T cell responses in PBMCs from both healthy donors and cancer patients. Importantly, SATB1565–574-specific T cells recognized and killed HLA-A*02+ SATB1+ cancer cells in an HLA-I-restricted manner.

Conclusions-Significance

We have identified a novel HLA-A*02-restricted SATB1-derived peptide epitope recognized by CD8+ T cells, which, in turn, recognizes and kills HLA-A*02+ SATB1+ tumor cells. The SATB1-derived epitope identified may be used as a diagnostic marker as well as an immune target for development of cancer vaccines.



Author: Mingjun Wang , Bingnan Yin , Satoko Matsueda , Lijuan Deng, Ying Li, Wei Zhao, Jia Zou, Qingtian Li, Christopher Loo, Rong-Fu Wan

Source: http://plos.srce.hr/



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