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149 results on '"Legut, Mateusz"'

1. Targeting of multiple tumor-associated antigens by individual T cell receptors during successful cancer immunotherapy

Author

Dolton, Garry, Rius, Cristina, Wall, Aaron, Szomolay, Barbara, Bianchi, Valentina, Galloway, Sarah A.E., Hasan, Md Samiul, Morin, Théo, Caillaud, Marine E., Thomas, Hannah L., Theaker, Sarah, Tan, Li Rong, Fuller, Anna, Topley, Katie, Legut, Mateusz, Attaf, Meriem, Hopkins, Jade R., Behiry, Enas, Zabkiewicz, Joanna, Alvares, Caroline, Lloyd, Angharad, Rogers, Amber, Henley, Peter, Fegan, Christopher, Ottmann, Oliver, Man, Stephen, Crowther, Michael D., Donia, Marco, Svane, Inge Marie, Cole, David K., Brown, Paul E., Rizkallah, Pierre, and Sewell, Andrew K.

Published
2023
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7. Genome editing approaches for development of pan-population immunotherapies

Author

Legut, Mateusz

Subjects
616.99
Abstract

Background - T-cell based immunotherapy is the greatest recent breakthrough in cancer treatment, and can induce complete lasting remission. T-cells are capable of responding to a vast diversity of antigens via their hypervariable T-cell receptor (TCR). However, current immunotherapies rely on αβ T-cells which are restricted to person-specific Human Leukocyte Antigen (HLA) molecules presenting peptides from cancer-specific antigens. Thus, a given αβ TCR therapy is applicable only to a minority of patients. In contrast, γδ T-cells, and some αβ T-cells, recognise diverse cancer types regardless of the HLA type. The aims of my thesis were to investigate the potential of using non-HLA restricted T-cells and their receptors for cancer immunotherapy, and to develop tools to facilitate the study of non-HLA restricted T-cells for cancer treatment. Results – Initially, I developed a CRISPR/Cas9 method for generation of superior TCR transduced cells, in terms of their anticancer reactivity and antigen sensitivity, in comparison to TCR transduced cells generated by current clinical methodologies. Using this TCR replacement method I demonstrated that the anticancer reactivity of broadly cancer-reactive γδ T-cells derived from a variety of clinically relevant sources is dependent on their TCRs. I also used CRISPR/Cas9 genome editing to generate a panel of cancer cell lines deficient in known ligands of non-HLA restricted T-cells that can be used for initial dissection of their anticancer reactivity. Using this approach, I demonstrated that one of non-HLA restricted T-cell clones I procured recognised targets via CD1a. Finally, I developed a whole genome CRISPR/Cas9 pipeline for discovery of ligands and pathways essential for cancer cell recognition by non-HLA restricted T-cells. Conclusions – My research demonstrated that TCRs from broadly cancer-reactive T-cells can be used to re-direct primary T-cells to many cancer types regardless of their HLA type, paving the way for pan-population immunotherapy. The discovery of non-HLA ligands for broadly cancer-reactive T-cells can be achieved using whole genome and targeted CRISPR/Cas9 gene editing technology.

Published
2017

9. Genome-wide CRISPR–Cas9 screening reveals ubiquitous T cell cancer targeting via the monomorphic MHC class I-related protein MR1

Author

Crowther, Michael D., Dolton, Garry, Legut, Mateusz, Caillaud, Marine E., Lloyd, Angharad, Attaf, Meriem, Galloway, Sarah A. E., Rius, Cristina, Farrell, Colin P., Szomolay, Barbara, Ager, Ann, Parker, Alan L., Fuller, Anna, Donia, Marco, McCluskey, James, Rossjohn, Jamie, Svane, Inge Marie, Phillips, John D., and Sewell, Andrew K.

Published
2020
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13. Targeting the T cell receptor [beta]-chain constant region for immunotherapy of T cell malignancies

Author

Maciocia, Paul M, Wawrzyniecka, Patrycja A, Philip, Brian, Ricciardelli, Ida, Akarca, Ayse U, Onuoha, Shimobi C, Legut, Mateusz, Cole, David K, Sewell, Andrew K, Gritti, Giuseppe, Somja, Joan, Piris, Miguel A, Peggs, Karl S, Linch, David C, Marafioti, Teresa, and Pule, Martin A

Subjects
T cells -- Receptors, Antigen receptors, T cell -- Physiological aspects -- Genetic aspects -- Research, Non-Hodgkin's lymphomas -- Genetic aspects -- Care and treatment -- Research, Immunotherapy -- Research, Biological sciences, Health
Abstract

Mature T cell cancers are typically aggressive, treatment resistant and associated with poor prognosis. Clinical application of immunotherapeutic approaches has been limited by a lack of target antigens that discriminate malignant from healthy (normal) T cells. Unlike B cell depletion, pan-T cell aplasia is prohibitively toxic. We report a new targeting strategy based on the mutually exclusive expression of T cell receptor [beta]-chain constant domains 1 and 2 (TRBC1 and TRBC2). We identify an antibody with unique TRBC1 specificity and use it to demonstrate that normal and virus-specific T cell populations contain both TRBC1[sup.+] and TRBC2[sup.+] compartments, whereas malignancies are restricted to only one. As proof of concept for anti-TRBC immunotherapy, we developed anti-TRBC1 chimeric antigen receptor (CAR) T cells, which recognized and killed normal and malignant TRBC1[sup.+], but not TRBC2[sup.+], T cells in vitro and in a disseminated mouse model of leukemia. Unlike nonselective approaches targeting the entire T cell population, TRBC-targeted immunotherapy could eradicate a T cell malignancy while preserving sufficient normal T cells to maintain cellular immunity., Author(s): Paul M Maciocia [1]; Patrycja A Wawrzyniecka [1]; Brian Philip [1]; Ida Ricciardelli [2]; Ayse U Akarca [1]; Shimobi C Onuoha [3]; Mateusz Legut [4]; David K Cole [4]; [...]

Published
2017
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18. Author Correction: Genome-wide CRISPR–Cas9 screening reveals ubiquitous T cell cancer targeting via the monomorphic MHC class I-related protein MR1

Author

Crowther, Michael D., Dolton, Garry, Legut, Mateusz, Caillaud, Marine E., Lloyd, Angharad, Attaf, Meriem, Galloway, Sarah A. E., Rius, Cristina, Farrell, Colin P., Szomolay, Barbara, Ager, Ann, Parker, Alan L., Fuller, Anna, Donia, Marco, McCluskey, James, Rossjohn, Jamie, Svane, Inge Marie, Phillips, John D., and Sewell, Andrew K.

Published
2020
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22. Identification of Required Host Factors for SARS-CoV-2 Infection in Human Cells

Author

Daniloski, Zharko, primary, Jordan, Tristan X., additional, Wessels, Hans-Hermann, additional, Hoagland, Daisy A., additional, Kasela, Silva, additional, Legut, Mateusz, additional, Maniatis, Silas, additional, Mimitou, Eleni P., additional, Lu, Lu, additional, Geller, Evan, additional, Danziger, Oded, additional, Rosenberg, Brad R., additional, Phatnani, Hemali, additional, Smibert, Peter, additional, Lappalainen, Tuuli, additional, tenOever, Benjamin R., additional, and Sanjana, Neville E., additional

Published
2021
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26. TCR-induced alteration of primary MHC peptide anchor residue

Author

Madura, Florian, Rizkallah, Pierre J., Legut, Mateusz, Holland, Christopher J., Fuller, Anna, Bulek, Anna, Schauenburg, Andrea J., Trimby, Andrew, Hopkins, Jade R., Wells, Stephen A., Godkin, Andrew, Miles, John J., Sami, Malkit, Li, Yi, Liddy, Nathaniel, Jakobsen, Bent K., Loveridge, E. Joel, Cole, David K., and Sewell, Andrew K.

Abstract

The HLA‐A*02:01‐restricted decapeptide EAAGIGILTV, derived from melanoma antigen recognized by T‐cells‐1 (MART‐1) protein, represents one of the best‐studied tumor associated T‐cell epitopes, but clinical results targeting this peptide have been disappointing. This limitation may reflect the dominance of the nonapeptide, AAGIGILTV, at the melanoma cell surface. The decapeptide and nonapeptide are presented in distinct conformations by HLA‐A*02:01 and TCRs from clinically relevant T‐cell clones recognize the nonapeptide poorly. Here, we studied the MEL5 TCR that potently recognizes the nonapeptide. The structure of the MEL5‐HLA‐A*02:01‐AAGIGILTV complex revealed an induced fit mechanism of antigen recognition involving altered peptide–MHC anchoring. This “flexing” at the TCR–peptide–MHC interface to accommodate the peptide antigen explains previously observed incongruences in this well‐studied system and has important implications for future therapeutic approaches. Finally, this study expands upon the mechanisms by which molecular plasticity can influence antigen recognition by T cells.

Published
2019

28. Peptide-MHC class 1 tetramers can fail to detect relevant functional T cell clonotypes and underestimate antigen-reactive T cell populations

Author

Rius, Cristina, Attaf, Meriem, Tungatt, Katie, Bianchi, Valentina, Legut, Mateusz, Bovay, Amandine, Donia, Marco, Straten, Per thor, Peakman, Mark, Svane, Inge Marie, Ott, Sascha, Connor, Tom, Szomolay, Barbara, Dolton, Garry, and Sewell, Andrew K.

Subjects
chemical and pharmacologic phenomena
Abstract

Peptide-MHC (pMHC) multimers, usually used as streptavidin-based tetramers, have transformed the study of Ag-specific T cells by allowing direct detection, phenotyping, and enumeration within polyclonal T cell populations. These reagents are now a standard part of the immunology toolkit and have been used in many thousands of published studies. Unfortunately, the TCR-affinity threshold required for staining with standard pMHC multimer protocols is higher than that required for efficient T cell activation. This discrepancy makes it possible for pMHC multimer staining to miss fully functional T cells, especially where low-affinity TCRs predominate, such as in MHC class II-restricted responses or those directed against self-antigens. Several recent, somewhat alarming, reports indicate that pMHC staining might fail to detect the majority of functional T cells and have prompted suggestions that T cell immunology has become biased toward the type of cells amenable to detection with multimeric pMHC. We use several viral- and tumor-specific pMHC reagents to compare populations of human T cells stained by standard pMHC protocols and optimized protocols that we have developed. Our results confirm that optimized protocols recover greater populations of T cells that include fully functional T cell clonotypes that cannot be stained by regular pMHC-staining protocols. These results highlight the importance of using optimized procedures that include the use of protein kinase inhibitor and Ab cross-linking during staining to maximize the recovery of Ag-specific T cells and serve to further highlight that many previous quantifications of T cell responses with pMHC reagents are likely to have considerably underestimated the size of the relevant populations.

Published
2018

29. Peptide-MHC Class I Tetramers Can Fail To Detect Relevant Functional T Cell Clonotypes and Underestimate Antigen-Reactive T Cell Populations

Author

Rius, Cristina, Attaf, Meriem, Tungatt, Katie, Bianchi, Valentina, Legut, Mateusz, Bovay, Amandine, Donia, Marco, thor Straten, Per, Peakman, Mark, Svane, Inge Marie, Ott, Sascha, Connor, Tom, Szomolay, Barbara, Dolton, Garry, and Sewell, Andrew K.

Subjects
Herpesvirus 4, Human/immunology, Herpesvirus 4, Human, Cytomegalovirus/immunology, Melanoma/immunology, RNA-Binding Proteins/immunology, Receptors, Antigen, T-Cell, Cytomegalovirus, chemical and pharmacologic phenomena, CD8-Positive T-Lymphocytes, Lymphocyte Activation/immunology, Lymphocyte Activation, CD8-Positive T-Lymphocytes/immunology, Lymphocytes, Tumor-Infiltrating, Antigen Recognition and Responses, HLA-A2 Antigen, Tumor Cells, Cultured, Humans, Melanoma, Protein Kinase Inhibitors, Lymphocytes, Tumor-Infiltrating/immunology, HLA-A2 Antigen/immunology, Orthomyxoviridae/immunology, Protein Binding/immunology, Protein Kinase Inhibitors/metabolism, Receptors, Antigen, T-Cell/immunology, Staining and Labeling/methods, Staining and Labeling, RNA-Binding Proteins, Orthomyxoviridae, Protein Binding
Abstract

Peptide-MHC (pMHC) multimers, usually used as streptavidin-based tetramers, have transformed the study of Ag-specific T cells by allowing direct detection, phenotyping, and enumeration within polyclonal T cell populations. These reagents are now a standard part of the immunology toolkit and have been used in many thousands of published studies. Unfortunately, the TCR-affinity threshold required for staining with standard pMHC multimer protocols is higher than that required for efficient T cell activation. This discrepancy makes it possible for pMHC multimer staining to miss fully functional T cells, especially where low-affinity TCRs predominate, such as in MHC class II-restricted responses or those directed against self-antigens. Several recent, somewhat alarming, reports indicate that pMHC staining might fail to detect the majority of functional T cells and have prompted suggestions that T cell immunology has become biased toward the type of cells amenable to detection with multimeric pMHC. We use several viral- and tumor-specific pMHC reagents to compare populations of human T cells stained by standard pMHC protocols and optimized protocols that we have developed. Our results confirm that optimized protocols recover greater populations of T cells that include fully functional T cell clonotypes that cannot be stained by regular pMHC-staining protocols. These results highlight the importance of using optimized procedures that include the use of protein kinase inhibitor and Ab cross-linking during staining to maximize the recovery of Ag-specific T cells and serve to further highlight that many previous quantifications of T cell responses with pMHC reagents are likely to have considerably underestimated the size of the relevant populations.

Published
2018

30. Dual molecular mechanisms govern escape at immunodominant HLA A2-restricted HIV epitope

Author

Cole, David K., Fuller, Anna, Dolton, Garry, Zervoudi, Efthalia, Legut, Mateusz, Miles, Kim, Blanchfield, Lori, Madura, Florian, Holland, Christopher J., Bulek, Anna M., Bridgeman, John S., Miles, John J., Schauenburg, Andrea J. A., Beck, Konrad, Evavold, Brian D., Rizkallah, Pierre J., and Sewell, Andrew K.

Subjects
chemical and pharmacologic phenomena, R1
Abstract

Serial accumulation of mutations to fixation in the SLYNTVATL (SL9) immunodominant, HIV p17 Gag-derived, HLA A2-restricted CTL epitope produce the SLFNTIAVL triple mutant ‘ultimate’ escape variant. These mutations in solvent-exposed residues are believed to interfere with TCR recognition, although confirmation has awaited structural verification. Here, we solved a TCR co-complex structure with SL9 and the triple escape mutant to determine the mechanism of immune escape in this eminent system. We show that, in contrast to prevailing hypotheses, the main TCR contact residue is 4N and the dominant mechanism of escape is not via lack of TCR engagement. Instead, mutation of solvent exposed residues in the peptide destabilize the peptide-HLA and reduce peptide density at the cell surface. These results highlight the extraordinary lengths that HIV employs to evade detection by high-affinity TCRs with a broad peptide-binding footprint and necessitate reevaluation of this exemplar model of HIV TCR escape.

Published
2017

31. Expanding the CITE-seq tool-kit: Detection of proteins, transcriptomes, clonotypes and CRISPR perturbations with multiplexing, in a single assay

Author

Mimitou, Eleni, primary, Cheng, Anthony, additional, Montalbano, Antonino, additional, Hao, Stephanie, additional, Stoeckius, Marlon, additional, Legut, Mateusz, additional, Roush, Timothy, additional, Herrera, Alberto, additional, Papalexi, Efthymia, additional, Ouyang, Zhengquing, additional, Satija, Rahul, additional, Sanjana, Neville E., additional, Koralov, Sergei B, additional, and Smibert, Peter, additional

Published
2018
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32. Incorporation of Peptides Targeting EGFR and FGFR1 into the Adenoviral Fiber Knob Domain and Their Evaluation as Targeted Cancer Therapies

Author

Uusi-Kerttula, Hanni, Legut, Mateusz, Davies, James, Jones, Rachel, Hudson, Emma, Hanna, Louise, Stanton, Richard J., Chester, John D., and Parker, Alan L.

Subjects
Ovarian Neoplasms, viruses, Recombinant Fusion Proteins, Genetic Vectors, Gene Transfer Techniques, Gene Expression, Genetic Therapy, Antibodies, Neutralizing, Adenoviridae, Cell Line, ErbB Receptors, Neutralization Tests, Transduction, Genetic, Neoplasms, Animals, Humans, Receptors, Virus, Capsid Proteins, Female, Receptor, Fibroblast Growth Factor, Type 1, Transgenes, Peptides, Research Articles
Abstract

Oncolytic virotherapies based on adenovirus 5 (Ad5) hold promise as adjunctive cancer therapies; however, their efficacy when delivered systemically is hampered by poor target cell specificity and preexisting anti-Ad5 immunity. Ovarian cancer represents a promising target for virotherapy, since the virus can be delivered locally into the peritoneal cavity. Both epidermal growth factor receptor (EGFR) and fibroblast growth factor receptor 1 (FGFR1) are overexpressed in the majority of human tumors, including ovarian cancer. To generate adenoviral vectors with improved tumor specificity, we generated a panel of Ad5 vectors with altered tropism for EGFR and FGFR, rather than the natural Ad5 receptor, hCAR. We have included mutations within AB loop of the viral fiber knob (KO1 mutation) to preclude interaction with hCAR, combined with insertions in the HI loop to incorporate peptides that bind either EGFR (peptide YHWYGYTPQNVI, GE11) or FGFR1 (peptides MQLPLAT, M*, and LSPPRYP, LS). Viruses were produced to high titers, and the integrity of the fiber protein was validated by Western blotting. The KO1 mutation efficiently ablated hCAR interactions, and significantly increased transduction was observed in hCARlow/EGFRhigh cell lines using Ad5.GE11, while transduction levels using Ad5.M* or Ad5.LS were not increased. In the presence of physiological concentrations of human blood clotting factor X (hFX), significantly increased levels of transduction via the hFX-mediated pathway were observed in cell lines, but not in primary tumor cells derived from epithelial ovarian cancer (EOC) ascites samples. Ad5-mediated transduction of EOC cells was completely abolished by the presence of 2.5% serum from patients, while, surprisingly, incorporation of the GE11 peptide resulted in significant evasion of neutralization in the same samples. We thus speculate that incorporation of the YHWYGYTPQNVI dodecapeptide within the fiber knob domain may provide a novel means of circumventing preexisting Ad5 immunity that warrants further investigation.

Published
2015

33. Nonstimulatory peptide–MHC enhances human T-cell antigen-specific responses by amplifying proximal TCR signaling

Author

Zhao, Xiang, primary, Sankaran, Shvetha, additional, Yap, Jiawei, additional, Too, Chien Tei, additional, Ho, Zi Zong, additional, Dolton, Garry, additional, Legut, Mateusz, additional, Ren, Ee Chee, additional, Sewell, Andrew K., additional, Bertoletti, Antonio, additional, MacAry, Paul A., additional, Brzostek, Joanna, additional, and Gascoigne, Nicholas R. J., additional

Published
2018
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34. Peptide–MHC Class I Tetramers Can Fail To Detect Relevant Functional T Cell Clonotypes and Underestimate Antigen-Reactive T Cell Populations

Author

Rius, Cristina, primary, Attaf, Meriem, additional, Tungatt, Katie, additional, Bianchi, Valentina, additional, Legut, Mateusz, additional, Bovay, Amandine, additional, Donia, Marco, additional, thor Straten, Per, additional, Peakman, Mark, additional, Svane, Inge Marie, additional, Ott, Sascha, additional, Connor, Tom, additional, Szomolay, Barbara, additional, Dolton, Garry, additional, and Sewell, Andrew K., additional

Published
2018
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35. Targeting the T cell receptor β-chain constant region for immunotherapy of T cell malignancies

Author

Maciocia, Paul M, primary, Wawrzyniecka, Patrycja A, additional, Philip, Brian, additional, Ricciardelli, Ida, additional, Akarca, Ayse U, additional, Onuoha, Shimobi C, additional, Legut, Mateusz, additional, Cole, David K, additional, Sewell, Andrew K, additional, Gritti, Giuseppe, additional, Somja, Joan, additional, Piris, Miguel A, additional, Peggs, Karl S, additional, Linch, David C, additional, Marafioti, Teresa, additional, and Pule, Martin A, additional

Published
2017
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36. PD-1+ Polyfunctional T Cells Dominate the Periphery after Tumor-Infiltrating Lymphocyte Therapy for Cancer

Author

Donia, Marco, primary, Kjeldsen, Julie Westerlin, additional, Andersen, Rikke, additional, Westergaard, Marie Christine Wulff, additional, Bianchi, Valentina, additional, Legut, Mateusz, additional, Attaf, Meriem, additional, Szomolay, Barbara, additional, Ott, Sascha, additional, Dolton, Garry, additional, Lyngaa, Rikke, additional, Hadrup, Sine Reker, additional, Sewell, Andrew K., additional, and Svane, Inge Marie, additional

Published
2017
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37. PD-1+ Polyfunctional T Cells Dominate the Periphery after Tumor-Infiltrating Lymphocyte Therapy for Cancer

Author

Donia, Marco, Kjeldsen, Julie Westerlin, Andersen, Rikke, Westergaard, Marie Christine Wulff, Bianchi, Valentina, Legut, Mateusz, Attaf, Meriem, Szomolay, Barbara, Ott, Sascha, Dolton, Garry, Lyngaa, Rikke, Hadrup, Sine Reker, Sewell, Andrew K, Svane, Inge Marie, Donia, Marco, Kjeldsen, Julie Westerlin, Andersen, Rikke, Westergaard, Marie Christine Wulff, Bianchi, Valentina, Legut, Mateusz, Attaf, Meriem, Szomolay, Barbara, Ott, Sascha, Dolton, Garry, Lyngaa, Rikke, Hadrup, Sine Reker, Sewell, Andrew K, and Svane, Inge Marie

Abstract

Purpose: Infusion of highly heterogeneous populations of autologous tumor-infiltrating lymphocytes (TIL) can result in tumor regression of exceptional duration. Initial tumor regression has been associated with persistence of tumor-specific TILs 1 month after infusion, but mechanisms leading to long-lived memory responses are currently unknown. Here, we studied the dynamics of bulk tumor-reactive CD8+ T-cell populations in patients with metastatic melanoma following treatment with TILs.Experimental Design: We analyzed the function and phenotype of tumor-reactive CD8+ T cells contained in serial blood samples of 16 patients treated with TILs.Results: Polyfunctional tumor-reactive CD8+ T cells accumulated over time in the peripheral lymphocyte pool. Combinatorial analysis of multiple surface markers (CD57, CD27, CD45RO, PD-1, and LAG-3) showed a unique differentiation pattern of polyfunctional tumor-reactive CD8+ T cells, with highly specific PD-1 upregulation early after infusion. The differentiation and functional status appeared largely stable for up to 1 year after infusion. Despite some degree of clonal diversification occurring in vivo within the bulk tumor-reactive CD8+ T cells, further analyses showed that CD8+ T cells specific for defined tumor antigens had similar differentiation status.Conclusions: We demonstrated that tumor-reactive CD8+ T-cell subsets that persist after TIL therapy are mostly polyfunctional, display a stable partially differentiated phenotype, and express high levels of PD-1. These partially differentiated PD-1+ polyfunctional TILs have a high capacity for persistence and may be susceptible to PD-L1/PD-L2-mediated inhibition. Clin Cancer Res; 23(19); 5779-88. ©2017 AACR.

Published
2017

38. The T cell antigen receptor: the Swiss army knife of the immune

Author

Attaf, Meriem, Legut, Mateusz, Cole, David, and Sewell, Andrew K.

Subjects
QR180, chemical and pharmacologic phenomena
Abstract

The mammalian T cell receptor (TCR) orchestrates immunity by responding\ud to many billions of different ligands that it has never encountered before\ud and cannot adapt to at the protein sequence level. This remarkable receptor\ud exists in two main heterodimeric isoforms: ab TCR and gd TCR. The ab\ud TCR is expressed on the majority of peripheral T cells. Most ab T cells\ud recognize peptides, derived from degraded proteins, presented at the cell\ud surface in molecular cradles called major histocompatibility complex (MHC)\ud molecules. Recent reports have described other ab T cell subsets. These\ud ‘unconventional’ T cells bear TCRs that are capable of recognizing lipid\ud ligands presented in the context of the MHC-like CD1 protein family or\ud bacterial metabolites bound to the MHC-related protein 1 (MR1). gd T cells\ud constitute a minority of the T cell pool in human blood, but can represent\ud up to half of total T cells in tissues such as the gut and skin. The identity\ud of the preferred ligands for gd T cells remains obscure, but it is now\ud known that this receptor can also functionally engage CD1-lipid, or\ud immunoglobulin (Ig) superfamily proteins called butyrophilins in the\ud presence of pyrophosphate intermediates of bacterial lipid biosynthesis.\ud Interactions between TCRs and these ligands allow the host to discriminate\ud between self and non-self and co-ordinate an attack on the latter. Here, we\ud describe how cells of the T lymphocyte lineage and their antigen receptors\ud are generated and discuss the various modes of antigen recognition by these\ud extraordinarily versatile receptors.

Published
2015

39. Partially differentiated polyfunctional T cells dominate the periphery after tumor-infiltrating lymphocytes therapy for cancer

Author

Donia, Marco, Westerlin Kjeldsen, Julie, Andersen, Rikke, Wulff Westergaard, Marie Christine, Bianchin, Valentina, Legut, Mateusz, Dolton, Garry, Szomolay, Barbara, Ott, Sascha, Lyngaa, Rikke Birgitte, Hadrup, Sine Reker, Kelvin Sewell, Andrew, Marie Svane, Inge, Donia, Marco, Westerlin Kjeldsen, Julie, Andersen, Rikke, Wulff Westergaard, Marie Christine, Bianchin, Valentina, Legut, Mateusz, Dolton, Garry, Szomolay, Barbara, Ott, Sascha, Lyngaa, Rikke Birgitte, Hadrup, Sine Reker, Kelvin Sewell, Andrew, and Marie Svane, Inge

Published
2016

40. Anacardic acid enhances the anticancer activity of liposomal mitoxantrone towards melanoma cell lines – in vitro studies [Corrigendum]

Author

Legut,Mateusz, Lipka,Dominik, Filipczak,Nina, Gubernator,Jerzy, Piwoni,Adriana, Kozubek,Arkadiusz, Legut,Mateusz, Lipka,Dominik, Filipczak,Nina, Gubernator,Jerzy, Piwoni,Adriana, and Kozubek,Arkadiusz

Abstract

Anacardic acid enhances the anticancer activity of liposomal mitoxantrone towards melanoma cell lines – in vitro studies [Corrigendum]Legut M, Lipka D, Filipczak N, et al. Int J Nanomedicine. 2014;9:653–668.The authors advise the Acknowledgment on page 666 is missing the final sentence:This study was supported by: the WrocÅ‚aw Research Centre EIT+ under the Biotechnologies and Advanced Medical Technologies project; BioMed (POIG.01.01.02-02-003/08), financed by the European Regional Development Fund (Operational Programme Innovative Economy, 1.1.2) #8221.Read the original article

Published
2015

41. Nonstimulatory peptide–MHC enhances human T-cell antigen-specific responses by amplifying proximal TCR signaling.

Author

Xiang Zhao, Sankaran, Shvetha, Jiawei Yap, Chien Tei Too, Zi Zong Ho, Dolton, Garry, Legut, Mateusz, Ee Chee Ren, Sewell, Andrew K., Bertoletti, Antonio, MacAry, Paul A., Brzostek, Joanna, and Gascoigne, Nicholas R. J.

Abstract

Foreign antigens are presented by antigen-presenting cells in the presence of abundant endogenous peptides that are nonstimulatory to the T cell. In mouse T cells, endogenous, nonstimulatory peptides have been shown to enhance responses to specific peptide antigens, a phenomenon termed coagonism. However, whether coagonism also occurs in human T cells is unclear, and the molecular mechanism of coagonism is still under debate since CD4 and CD8 coagonism requires different interactions. Here we show that the nonstimulatory, HIV-derived peptide GAG enhances a specific human cytotoxic T lymphocyte response to HBV-derived epitopes presented by HLA-A*02:01. Coagonism in human T cells requires the CD8 coreceptor, but not T-cell receptor (TCR) binding to the nonstimulatory peptide–MHC. Coagonists enhance the phosphorylation and recruitment of several molecules involved in the TCR-proximal signaling pathway, suggesting that coagonists promote T-cell responses to antigenic pMHC by amplifying TCR-proximal signaling. [ABSTRACT FROM AUTHOR]

Published
2018
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43. Anacardic acid enhances the anticancer activity of liposomal mitoxantrone towards melanoma cell lines – in vitro studies

Author

Legut,Mateusz, Lipka,Dominik, Filipczak,Nina, Piwoni,Adriana, Kozubek,Arkadiusz, Gubernator,Jerzy, Legut,Mateusz, Lipka,Dominik, Filipczak,Nina, Piwoni,Adriana, Kozubek,Arkadiusz, and Gubernator,Jerzy

Abstract

Mateusz Legut, Dominik Lipka, Nina Filipczak, Adriana Piwoni, Arkadiusz Kozubek, Jerzy GubernatorDepartment of Lipids and Liposomes, Faculty of Biotechnology, University of WrocÅ‚aw, WrocÅ‚aw, PolandAbstract: This paper describes a novel formulation of antineoplastic drug: mitoxantrone loaded into liposomal carriers enriched with encapsulated anacardic acid in the liposomal bilayer using a vitamin C gradient. Anacardic acid is a potent epigenetic agent with anticancer activity. This is the first liposomal formulation to combine an actively encapsulated drug and anacardic acid. The liposomes were characterized in terms of basic parameters, such as size, zeta potential, optimal drug-to-lipid ratio, loading time and temperature, and stability at 4°C and in human plasma in vitro. The formulation was found to be stable, and the loading process was rapid and efficient (drug-to-lipid ratio of up to 0.3 with over 90% efficiency in 5 minutes). The cytotoxicity of these formulations was assessed using the human melanoma cell lines A375 and Hs294T and the normal human dermal fibroblast line. The results showed that anacardic acid and to a smaller extent vitamin C significantly increased the cytotoxicity of the drug towards melanoma compared to ammonium sulfate liposomes. On the other hand, vitamin C and anacardic acid both protected normal cells from damage caused by the drug. The formulation combining anacardic acid, vitamin C, and mitoxantrone showed promising results in terms of cytotoxicity and cytoprotection. Therefore, it has potential for anticancer treatment.Keywords: anacardic acid, vitamin C, ascorbic acid, liposomes, mitoxantrone, melanomaCorrigendum for this paper has been published&nbsp

Published
2014

45. Vitamin C-driven epirubicin loading into liposomes

Author

Lipka,Dominik, Gubernator,Jerzy, Filipczak,Nina, Barnert,Sabine, Süss,Regine, Legut,Mateusz, Kozubek,Arkadiusz, Lipka,Dominik, Gubernator,Jerzy, Filipczak,Nina, Barnert,Sabine, Süss,Regine, Legut,Mateusz, and Kozubek,Arkadiusz

Abstract

Dominik Lipka,1 Jerzy Gubernator,1 Nina Filipczak,1 Sabine Barnert,2 Regine Süss,2 Mateusz Legut,1 Arkadiusz Kozubek1 1Department of Lipids and Liposomes, University of Wroclaw, Wroclaw, Poland; 2Department of Pharmaceutical Technology, Albert Ludwigs University, Freiburg, Germany Abstract: The encapsulation of anticancer drugs in a liposome structure protects the drug during circulation and increases drug accumulation in the cancer tissue and antitumor activity while decreasing drug toxicity. This paper presents a new method of active drug loading based on a vitamin C pH/ion gradient. Formulations were characterized in terms of the following parameters: optimal external pH, time and drug-to-lipid ratio for the purpose of remote loading, and in vitro stability. In the case of the selected drug, epirubicin (EPI), its coencapsulation increases its anticancer activity through a possibly synergistic effect previously reported by other groups for a free nonencapsulated drug/vitamin C cocktail. The method also has another advantage over other remote-loading methods: it allows faster drug release through liposome destabilization at the tumor site, thanks to the very good solubility of the EPI vitamin C salt, as seen on cryogenic transmission electron microscopy images. This influences the drug-release process and increases the anticancer activity of the liposome formulation. The liposomes are characterized as stable, with very good pharmacokinetics (half-life 18.6 hours). The antitumor activity toward MCF-7 and 4T-1 breast cancer cells was higher in the case of EPI loaded via our gradient than via an ammonium sulfate gradient. Finally, the EPI liposomal formulation and the free drug were tested using the murine 4T-1 breast cancer model. The antitumor activity of the encapsulated drug was confirmed (tumor-growth inhibition over 40% from day 16 until the end of the experiment), and the free drug was shown to have no anticancer activity at the tested dose. Keywords

Published
2013

47. 31st Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2016): part one: National Harbor, MD, USA. 9-13 November 2016

Author

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Published
2016
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49. TCR‐induced alteration of primary MHC peptide anchor residue

Author

Madura, Florian, Rizkallah, Pierre J., Legut, Mateusz, Holland, Christopher J., Fuller, Anna, Bulek, Anna, Schauenburg, Andrea J., Trimby, Andrew, Hopkins, Jade R., Wells, Stephen A., Godkin, Andrew, Miles, John J., Sami, Malkit, Li, Yi, Liddy, Nathaniel, Jakobsen, Bent K., Loveridge, E. Joel, Cole, David K., and Sewell, Andrew K.

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