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The endoplasmic reticulum (ER) is an organelle crucial to many cellular functions and processes, including the mounting of T-cell immune responses. Indeed, the ER has a well-established central role in anti-tumor immunity. Perhaps best characterized is the role of the ER in the processing of antigen peptides and the subsequent peptide assembly into MHC class I and II molecules. Such MHC/tumor-derived peptide complexes are pivotal for the correct recognition of altered self or viral peptides and the subsequent clonal expansion of tumor-reactive T-cells. In line with the role of the ER in immunity, tumor-associated mutations in ER proteins, as well as ER protein content and localization can have both deleterious and advantageous effects on anti-tumor immune responses. For instance, loss of function of ER-aminopeptidases, that trim peptides to size for MHC, alter the MHC class I - peptide repertoire thereby critically and negatively affecting T-cell recognition. On the other hand, altered localization of ER proteins can have immune-promoting effects. Specifically, translocation of certain ER proteins to the cell surface has been shown to promote anti-tumor T-cell immunity by directing uptake of apoptotic tumor cells to professional antigen presenting cells, thereby facilitating anti-tumor T-cell immunity. These selected examples highlight a diverse and multi-faceted role of the ER in anti-tumor immunity. Molecular biological insights from the past decade have uncovered that ER components may affect tumor immunity and have invoked a variety of follow-up questions. For instance, how and why are ER proteins over-expressed in tumors? How do nucleotide and somatic mutations in ER chaperones/processing machinery affect the MHC/peptide complex and tumor cell immunogenicity? How do ER-proteins translocate to the cell surface? What if any is the potential role of extracellular ER protein in tumor immunotherapy/vaccines, and can they be delivered to the tumor cell surface by photodynamic therapy, anthracyclines or by other means? In this special research topics issue, we welcome basic and clinical research reports covering all aspects of ER proteins in cancer recognition by the immune system, therapy and drug development. We also welcome reports describing new insights into ER stress, signalling and homeostasis in immunogenic cell death in cancer, the effect of parasitic ER proteins on tumour growth, ER protein regulation of angiogenesis. Submission of original research articles, perspective, reviews and topical comments is encouraged. We aim to provide a comprehensive series of articles that will aid our understanding in a new and exiting avenue of tumour immunology and therapeutic development, exploiting a collection of proteins within the ER that are not obvious candidates for immunity to tumors.

Endoplasmic reticulum. --- Tumors --- Immunology. --- Oncology. --- Endoplasmic Reticulum Stress. --- Autoimmunity --- Angiogenesis --- T-cell receptors --- genome damage --- phage display --- Aminopeptidases --- Grp170 --- Oxidoreductases --- Vaccines --- chaperones --- Immunological aspects. --- Autoimmunity --- Angiogenesis --- T-cell receptors --- genome damage --- phage display --- Aminopeptidases --- Grp170 --- Oxidoreductases --- Vaccines --- chaperones

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The endoplasmic reticulum (ER) is an organelle crucial to many cellular functions and processes, including the mounting of T-cell immune responses. Indeed, the ER has a well-established central role in anti-tumor immunity. Perhaps best characterized is the role of the ER in the processing of antigen peptides and the subsequent peptide assembly into MHC class I and II molecules. Such MHC/tumor-derived peptide complexes are pivotal for the correct recognition of altered self or viral peptides and the subsequent clonal expansion of tumor-reactive T-cells. In line with the role of the ER in immunity, tumor-associated mutations in ER proteins, as well as ER protein content and localization can have both deleterious and advantageous effects on anti-tumor immune responses. For instance, loss of function of ER-aminopeptidases, that trim peptides to size for MHC, alter the MHC class I - peptide repertoire thereby critically and negatively affecting T-cell recognition. On the other hand, altered localization of ER proteins can have immune-promoting effects. Specifically, translocation of certain ER proteins to the cell surface has been shown to promote anti-tumor T-cell immunity by directing uptake of apoptotic tumor cells to professional antigen presenting cells, thereby facilitating anti-tumor T-cell immunity. These selected examples highlight a diverse and multi-faceted role of the ER in anti-tumor immunity. Molecular biological insights from the past decade have uncovered that ER components may affect tumor immunity and have invoked a variety of follow-up questions. For instance, how and why are ER proteins over-expressed in tumors? How do nucleotide and somatic mutations in ER chaperones/processing machinery affect the MHC/peptide complex and tumor cell immunogenicity? How do ER-proteins translocate to the cell surface? What if any is the potential role of extracellular ER protein in tumor immunotherapy/vaccines, and can they be delivered to the tumor cell surface by photodynamic therapy, anthracyclines or by other means? In this special research topics issue, we welcome basic and clinical research reports covering all aspects of ER proteins in cancer recognition by the immune system, therapy and drug development. We also welcome reports describing new insights into ER stress, signalling and homeostasis in immunogenic cell death in cancer, the effect of parasitic ER proteins on tumour growth, ER protein regulation of angiogenesis. Submission of original research articles, perspective, reviews and topical comments is encouraged. We aim to provide a comprehensive series of articles that will aid our understanding in a new and exiting avenue of tumour immunology and therapeutic development, exploiting a collection of proteins within the ER that are not obvious candidates for immunity to tumors.

Endoplasmic reticulum. --- Tumors --- Immunology. --- Oncology. --- Endoplasmic Reticulum Stress. --- Immunological aspects. --- Autoimmunity --- Angiogenesis --- T-cell receptors --- genome damage --- phage display --- Aminopeptidases --- Grp170 --- Oxidoreductases --- Vaccines --- chaperones

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This volume provides a comprehensive compilation of protocols in T cell repertoire analysis, from the leading experts in the field, representing both well-established methods and cutting-edge advances. Chapters broadly cover the emerging new T cell subsets, sequencing technologies for capturing TCR repertoire, and computational tools for analyzing an ever-growing TCR repertoire, with a particular focus on how to link the sequence with TCR antigen specificity. Written in the successful Methods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible protocols, and notes on troubleshooting and avoiding known pitfalls. Authoritative and cutting-edge, T-Cell Repertoire Characterization aims to be a useful practical guide to researches to help further their study in this field. .

Immunology. --- Cytology. --- Cancer. --- Cell Biology. --- Cancers. --- Cancers --- Carcinoma --- Malignancy (Cancer) --- Malignant tumors --- Tumors --- Cell biology --- Cellular biology --- Biology --- Cells --- Immunobiology --- Life sciences --- Serology --- T cells --- Receptors --- T cell receptors --- T lymphocyte antigen receptors --- Cell receptors

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For decades, T cells were thought to solely respond to protein-derived antigens. However, the discovery of the CD1 antigen presenting system shows how antigen presenting cells can display lipid antigens to T cells. Crystal structures show that CD1 proteins accomplish this function by inserting lipids into a hydrophobic groove on the distal surface of the protein, forming CD1-lipid complexes that act as ligands for T cell receptors. CD1-reactive T cells with conserved (NK T cells) or diverse T cell receptors possess cytokine secretion and other effector mechanisms that influence many aspects of immune response. There is increasing evidence that the CD1 system has been conserved throughout mammalian evolution and is capable of presenting structurally diverse diacyglycerol, sphingolipid, polyisoprenol and lipopeptide antigens. These features of CD1 antigen presentation systems now point to a new and expanded view of the natural function of ab T cells, which involves surveillance of both the protein and lipid components of target cells. Further, cellular systems that were previously considered to have functions in lipid metabolism can now be studied in context of their immunological functions. This volume provides a comprehensive discussion of these basic aspects of CD1 biology and summarizes the most recent research into the role of CD1 in infectious, autoimmune, allergic and neoplastic disease.

CD antigens. --- T cells --- Receptors. --- T cell receptors --- T lymphocyte antigen receptors --- Cell receptors --- Antigens, CD --- CD glycoproteins --- CD molecules --- CD receptors --- CD surface immunoglobulin ligands --- Differentiation antigens, Human leukocyte --- Human leukocyte differentiation antigens --- Leukocyte differentiation antigens, Human --- Cell surface antigens --- Fc receptors --- Glycoproteins --- Immunology. --- Immunobiology --- Life sciences --- Serology

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T cells --- Tumor antigens. --- Receptors, Chimeric Antigen --- Neoplasms --- Immunotherapy, Adoptive. --- Receptors, Antigen, T-Cell. --- Cell- and Tissue-Based Therapy. --- Receptors. --- therapeutic use. --- therapy. --- Therapy, Cell --- Therapy, Tissue --- Cell Therapy --- Tissue Therapy --- Cell and Tissue Based Therapy --- Tissue Therapy, Historical --- Receptors, T-Cell Antigen --- T-Cell Antigen Receptor --- T-Cell Receptor --- Antigen Receptors, T-Cell --- T-Cell Receptors --- Antigen Receptor, T-Cell --- Antigen Receptors, T Cell --- Receptor, T-Cell --- Receptor, T-Cell Antigen --- Receptors, T Cell Antigen --- Receptors, T-Cell --- T Cell Antigen Receptor --- T Cell Receptor --- T Cell Receptors --- T-Cell Antigen Receptors --- CD3 Complex --- Genes, T-Cell Receptor --- Complementarity Determining Regions --- Adoptive Immunotherapy --- CAR T-Cell Therapy --- Cellular Immunotherapy, Adoptive --- Chimeric Antigen Receptor Therapy --- Immunotherapy, Adoptive Cellular --- Adoptive Cellular Immunotherapy --- Adoptive Cellular Immunotherapies --- Adoptive Immunotherapies --- CAR T Cell Therapy --- CAR T-Cell Therapies --- Cellular Immunotherapies, Adoptive --- Immunotherapies, Adoptive --- Immunotherapies, Adoptive Cellular --- T-Cell Therapies, CAR --- T-Cell Therapy, CAR --- Therapies, CAR T-Cell --- Therapy, CAR T-Cell --- Killer Cells, Lymphokine-Activated --- Cytapheresis --- Lymphocytes, Tumor-Infiltrating --- Monocytes, Activated Killer --- Antigens --- Tumor markers --- T cell receptors --- T lymphocyte antigen receptors --- Cell receptors