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• W2896578754 endingPage "936" @default.
• W2896578754 startingPage "921" @default.
• W2896578754 abstract "Recent advances in omics and laboratory techniques provide immune genomic and proteomic data, which, with the newest analysis tools, may aid in the development of more safe and effective cancer AT with TCR-engineered T cells. Novel algorithms that surpass the mere binding of tumor epitopes to HLA-I and integrate multiple immune parameters, including immunopeptidomes and TCR–peptide binding modes, are expected to accelerate the selection of valid target epitopes and corresponding TCRs for AT. Immunophenotyping combining in silico and laboratory techniques, including multiplex imaging, is required to identify shortcomings in T cell immunity in tumors, and to provide rationales for designing combination AT. An objective is that patient subgroups be defined according to epitopes, TCRs, and immune evasive mechanisms to maximally sensitize the tumor for T cells, while at the same time putting patients at minimal risk for treatment-related side effects. Adoptive transfer of TCR-engineered T cells is a potent therapy, able to induce clinical responses in different human malignancies. Nevertheless, treatment toxicities may occur and, in particular for solid tumors, responses may be variable and often not durable. To address these challenges, it is imperative to carefully select target antigens and to immunologically interrogate the corresponding tumors when designing optimal T cell therapies. Here, we review recent advances, covering both omics- and laboratory tools that can enable the selection of optimal T cell epitopes and TCRs as well as the identification of dominant immune evasive mechanisms within tumor tissues. Furthermore, we discuss how these techniques may aid in a rational design of effective combinatorial adoptive T cell therapies. Adoptive transfer of TCR-engineered T cells is a potent therapy, able to induce clinical responses in different human malignancies. Nevertheless, treatment toxicities may occur and, in particular for solid tumors, responses may be variable and often not durable. To address these challenges, it is imperative to carefully select target antigens and to immunologically interrogate the corresponding tumors when designing optimal T cell therapies. Here, we review recent advances, covering both omics- and laboratory tools that can enable the selection of optimal T cell epitopes and TCRs as well as the identification of dominant immune evasive mechanisms within tumor tissues. Furthermore, we discuss how these techniques may aid in a rational design of effective combinatorial adoptive T cell therapies. non self-allele which can be recognized by TCRs independent of the bound peptide. a sequence of operations in computer science, such as calculating, data processing, and automated reasoning. binding strength based on multiple receptor target interactions (for instance, T cell avidity includes combination of TCR–peptide: MHC and CD8). class of tumor antigens with expression restricted to immune privileged tissues (germline) and tumors. T cells engineered to express a chimeric antigen receptor consisting of an extracellular antibody-domain, an intracellular TCR domain, and often a co-stimulatory domain. a defined stretch of amino acids (9–11 amino acids) that is derived from intracellular proteins and is specifically recognized by a TCR. After processing by the (immune-) proteasome, peptides are presented by MHC molecules on the cell surface of target cells to the TCR on the cell surface of T cells. chain reaction of protein cleavage that can result in the activation of immune cells. T cell reactivity against an epitope other than the cognate epitope (often highly similar to cognate epitope and recognized with lower TCR affinity). class of tumor antigens that are expressed at different stages of tissue development or cell activation. inactive state of endothelial cells, generally with limited expression of chemokines, adhesion molecules, and co-stimulatory ligands, and consequently not favoring tissue entry of T cells. receptors and ligands that, upon ligation, result in limiting activation of immune cells (i.e., putting immune cells in check). interplay between tumors and immune system, resulting in loss of antigen-positive tumor cells upon selective pressure by T cells. cells, including immune cells but also stromal cells, such as CAF, that can limit T cell function. collection of all presented peptides by MHC molecules of a target cell(s) or tissue. assessment of immunogenicity and immune evasive mechanisms by omics and/or laboratory tools. innate immune cells that normally are specialized in engulfing aberrant cells and presenting antigens, but due to polarization, which may be a consequence of the tumor microenvironment, become immune suppressor cells. class of tumor antigens that are derived from mutated proteins. method of high-throughput sequencing of nucleic acids. toxicity due to crossreactive T cells recognizing an epitope very similar to the cognate epitope outside tumor tissue. collection of sciences and necessary tools that focus on the structure, function, and related aspects of defined groups of molecules (genomics: DNA; transcriptomics: RNA; proteomics: proteins; metabolomics: metabolites; immunomics: immune markers, etc.). toxicity due to T cells targeting their cognate epitope outside tumor tissue. class of tumor antigens derived from viral genes that had been integrated into the DNA of (pre-)malignant cells. locating experimental nucleic acid sequences (called reads), through alignment with a set of reference sequences. number of sequences (called reads) that include a nucleotide of a reconstructed sequence, also referred to as coverage. technologies that enable targeted genome editing through different principles TALEN (transcription activator-like effector nucleases) relies on modified restriction enzymes to cut out specific sequences from DNA; whereas CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats) relies on guide RNA and a DNA endonuclease activity to remove specific sequences from DNA]. diversity and abundance of TCR genes (often represented by β chain) used as a measure of T cell clonality; the more skewed a TCR repertoire, the more clonal the T cell response has been. method to determine an ion’s mass-to-charge ratio via acceleration in a known electric field, by time measurement. natural or synthetic molecules that ligate to and stimulate toll-like receptors (TLR), the latter being evolutionary conserved receptors generally expressed on innate immune cells and taking part in the recognition of pathogen-associated molecular patterns. immune cells that are present in neoplastic tissue. expression of tumor antigens by cancerous tissue but not healthy tissue (immune privileged tissues represent an exception in case of CGAs). sequencing of all protein-coding genes of the genome." @default.
• W2896578754 created "2018-10-26" @default.
• W2896578754 creator A5060943632 @default.
• W2896578754 creator A5066477976 @default.
• W2896578754 creator A5066926133 @default.
• W2896578754 creator A5069775632 @default.
• W2896578754 creator A5084751312 @default.
• W2896578754 date "2018-11-01" @default.
• W2896578754 modified "2023-09-27" @default.
• W2896578754 title "Adoptive T Cell Therapy: New Avenues Leading to Safe Targets and Powerful Allies" @default.
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