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Articles de revues sur le sujet « HLA knockout »

Auteur : Grafiati
Publié le 12 avril 2025

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1

McCarty, Todd M., Zhiwei Yu, Xiping Liu, Don J. Diamond, and Joshua D. I. Ellenhorn. "An HLA-restricted, p53 specific immune response from HLA transgenic p53 knockout mice." Annals of Surgical Oncology 5, no. 1 (1998): 93–99. http://dx.doi.org/10.1007/bf02303770.

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Suzuki, Daisuke, Naoshi Sugimoto, Norihide Yoshikawa, et al. "Natural Killer Cell Activities Against iPSCs-Derived HLA-Knockout Platelets and Megakaryocytes Reveal Perfect Rejection Profiles for Allotransfusion." Blood 128, no. 22 (2016): 3841. http://dx.doi.org/10.1182/blood.v128.22.3841.3841.

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Abstract Background Platelet transfusion refractoriness (PTR) due to immune factors occurs in 5-15% of thrombocytopenic patients who have received transfusions. The dominant cause of immune PTR is the production of allo-antibodies to human leukocyte antigen (HLA) class I, which is expressed on platelets. In current clinical settings, transfusion of HLA-compatible platelets is the only practical strategy, but their supply is weak due to limited donor source, gives excessive burden on specific donors, and requires increased efforts and costs. To overcome these issues, we plan to produce HLA-knoc
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Kwon, Yoo-Wook, Hyo-Suk Ahn, Jin-Woo Lee, et al. "HLA DR Genome Editing with TALENs in Human iPSCs Produced Immune-Tolerant Dendritic Cells." Stem Cells International 2021 (May 20, 2021): 1–14. http://dx.doi.org/10.1155/2021/8873383.

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Although human induced pluripotent stem cells (iPSCs) can serve as a universal cell source for regenerative medicine, the use of iPSCs in clinical applications is limited by prohibitive costs and prolonged generation time. Moreover, allogeneic iPSC transplantation requires preclusion of mismatches between the donor and recipient human leukocyte antigen (HLA). We, therefore, generated universally compatible immune nonresponsive human iPSCs by gene editing. Transcription activator-like effector nucleases (TALENs) were designed for selective elimination of HLA DR expression. The engineered nuclea
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Zha, Shijun, Johan Chin-Kang Tay, Sumin Zhu, Zhendong Li, Zhicheng Du та Shu Wang. "Generation of Mesenchymal Stromal Cells with Low Immunogenicity from Human PBMC-Derived β2 Microglobulin Knockout Induced Pluripotent Stem Cells". Cell Transplantation 29 (1 січня 2020): 096368972096552. http://dx.doi.org/10.1177/0963689720965529.

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Mesenchymal stromal cells (MSCs) are viewed as immune-privileged cells and have been broadly applied in allogeneic adoptive cell transfer for regenerative medicine or immune-suppressing purpose. However, the surface expression of human leukocyte antigen (HLA) class I molecules on MSCs could still possibly induce the rejection of allogeneic MSCs from the recipients. Here, we disrupted the β2 microglobulin ( B2M) gene in human peripheral blood mononuclear cell-derived induced pluripotent stem cells (iPSCs) with two clustered regulatory interspaced short palindromic repeat (CRISPR)-associated Cas
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Karkischenko, V. N., A. G. Berzina, I. A. Pomytkin, et al. "Immune Response in HLA-A*02:01 Transgenic Humanized Mice to the Introduction of Horse IgG Antigen." Journal Biomed 20, no. 2 (2024): 45–52. http://dx.doi.org/10.33647/2074-5982-20-2-45-52.

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The introduction of a transgene can impact negatively the functioning of vital systems in biomodels. We carried out a comparative analysis of the immune response of mice of the HLA-A*02:01 humanized transgenic line, mice with mouse β2-microglobulin gene knockout, and wild-type mice to the introduction of horse immunoglobulin as an antigen. The biomodel lines were created at the Scientific Center of Biomedical Technologies of the Federal Medical and Biological Agency of Russia. The maximum immune response was achieved on the 30th day from the onset of immunization in animals of the HLA-A*02:01
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Rivera González, Lorena, Yaritza Inostroza-Nieves, Alexandra Lozano, et al. "Endothelin-1 Regulates Molecules of the Major Histocompatibility Complex: Role in Sickle Cell Disease." Blood 128, no. 22 (2016): 3638. http://dx.doi.org/10.1182/blood.v128.22.3638.3638.

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Abstract Molecules of the Major Histocompatibility Complex (MHC), and in particular specific human leukocyte antigen (HLA) alleles, have been proposed in the pathophysiology of immune and vascular alterations leading to vasoocclusive crises (VOC) and stroke in Sickle Cell Disease (SCD). Endothelial cells express MHC molecules following exposure to cytokines. SCD is characterized, in part, by vascular endothelial cell activation, increased oxidative stress, sickle cell adhesion and excess levels of the potent mitogen, endothelin-1 (ET-1). ET-1 activates endothelial cells, induces oxidative stre
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Veldman, Johanna, Lydia Visser, Magdalena Huberts-Kregel, et al. "Rosetting T cells in Hodgkin lymphoma are activated by immunological synapse components HLA class II and CD58." Blood 136, no. 21 (2020): 2437–41. http://dx.doi.org/10.1182/blood.2020005546.

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Abstract A unique feature of Hodgkin lymphoma (HL) is the presence of CD4+ T cells that surround, protect, and promote survival of tumor cells. The adhesion molecules involved in this so-called T-cell rosetting are important components of the immunological synapse (IS). However, it is unknown whether this synapse is fully assembled and leads to T-cell activation by enabling interaction between the T-cell receptor (TCR) and human leukocyte antigen class II (HLA-II). We established a novel rosetting model by coculturing HLA-II–matched peripheral blood mononuclear cells with HL cell lines and sho
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Chen, Liye, Hui Shi, Jack Yuan, and Paul Bowness. "Position 97 of HLA-B, a residue implicated in pathogenesis of ankylosing spondylitis, plays a key role in cell surface free heavy chain expression." Annals of the Rheumatic Diseases 76, no. 3 (2016): 593–601. http://dx.doi.org/10.1136/annrheumdis-2016-209512.

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ObjectiveAssociation of position 97 (P97) residue polymorphisms in human leucocyte antigen (HLA)-B, including HLA-B*27, with ankylosing spondylitis (AS) has recently been reported. We studied the effect of P97 variations on cell surface expression of the AS-associated HLA-B*27 and HLA-B*51, and the AS-protective HLA-B*7.MethodsFlow cytometry was used to measure surface expression of HLA-B*27 in C1R/HeLa cells expressing HLA-B*27 (N97) and six mutants at P97 (N97T, N97S, N97V, N97R, N97W and N97D). Transporter associated with antigen processing-deficient T2, tapasin-deficient 220, β2m-deficient
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Torikai, Hiroki, Andreas Reik, Carrie Yuen, et al. "HLA and TCR Knockout by Zinc Finger Nucleases: Toward “off-the-Shelf” Allogeneic T-Cell Therapy for CD19+ Malignancies." Blood 116, no. 21 (2010): 3766. http://dx.doi.org/10.1182/blood.v116.21.3766.3766.

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Abstract Abstract 3766 Cell therapy by infusion of T cells can reconstitute immunity to combat pathogens and malignancies. However, the time required to manufacture T cells with the desired properties and in sufficient numbers ex vivo is often incompatible with the treatment window for patients. Furthermore, autologous T cells from patients with advanced disease may have compromised function and be tolerant to desired antigens. A potential solution would be an approach to infuse allogeneic T cells that avoids immune-mediated rejection caused by host T cells recognizing disparate major or minor
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Legut, Mateusz, Garry Dolton, Afsar Ali Mian, Oliver G. Ottmann, and Andrew K. Sewell. "CRISPR-mediated TCR replacement generates superior anticancer transgenic T cells." Blood 131, no. 3 (2018): 311–22. http://dx.doi.org/10.1182/blood-2017-05-787598.

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Key Points Endogenous TCR knockout increases the expression and functional activity of simultaneously transduced TCR (TCR replacement). TCR replacement results in superior targeting of hematological malignancies by T cells transduced with a non–HLA-restricted γδ TCR.
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Croom-Perez, Tayler J., Liza D. Robles-Carrillo, Md Faqrul Hasan, and Alicja J. Copik. "Abstract 2910: NKG2A suppression enhances the function of primary human Natural Killer cells." Cancer Research 83, no. 7_Supplement (2023): 2910. http://dx.doi.org/10.1158/1538-7445.am2023-2910.

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Abstract In this study we propose inhibition of NKG2A signaling enhances the anti-tumor response of primary human NK cells. One mechanism employed by tumor cells to evade immunosurveillance is through induction of the surface expression of unconventional HLA ligands that agonize inhibitory receptors on immune cells. Specifically on some tumors, HLA-E is either expressed or its expression is known to be induced by IFNγ and is indicative of resistance to immunotherapy. HLA-E agonizes the CD94/NKG2A inhibitory complex on NK cells and some T cells to lessen their cytotoxicity, potentially decreasi
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Krco, Christopher J., Shohei Watanabe, Jerry Harders, Marie M. Griffths, Harvinder Luthra, and Chella S. David. "Identification of T Cell Determinants on Human Type II Collagen Recognized by HLA-DQ8 and HLA-DQ6 Transgenic Mice." Journal of Immunology 163, no. 3 (1999): 1661–65. http://dx.doi.org/10.4049/jimmunol.163.3.1661.

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Abstract HLA-DQA1*0301 and HLA-DQB1*0302 genes encoding the HLA-DQ8 molecule and HLA-DQA1*0103 and HLA-DQB1*0601 genes encoding the HLA-DQ6 molecule were introduced into H-2Aβo knockout mice. Three lines of transgenic mice were established: HLA-DQ8, HLA-DQ6, and HLA-DQ8β6α. HLA-DQ8 mice are susceptible to collagen-induced arthritis, while HLA-DQ6 mice are resistant. HLA-DQ8β6α mice develop polychrondritis in addition to arthritis. Transgenic mice were primed and challenged with individual synthetic peptides representing human type II collagen. A total of 101 synthetic peptides were tested in e
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Neeno, T., C. J. Krco, J. Harders, J. Baisch, S. Cheng, and C. S. David. "HLA-DQ8 transgenic mice lacking endogenous class II molecules respond to house dust allergens: identification of antigenic epitopes." Journal of Immunology 156, no. 9 (1996): 3191–95. http://dx.doi.org/10.4049/jimmunol.156.9.3191.

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Abstract We have introduced HLA-DQ8 (HLADQB*0302 and HLA-DQA*0301) genes into A beta 0 knockout mice. Transgenic animals were immunized with a whole body extract of Dermatophagoides pteronyssinus (Der p), one of the causative agents of house dust mite allergy. Transgenic mice expressing HLA-DQ8 genes elicited HLA-DQ8-restricted responses driven by CD4+ T cells. Synthetic-overlapping peptides representing a major allergen of house dust mite (Der p 2) were synthesized and used as immunogens. HLA-DQ8+ mice responded to three peptides: 8 (residues 61-80), 11 (residues 91-110), and 13 (residues 111
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Karkischenko, V. N., V. A. Ezerskiy, E. M. Koloskova та M. S. Nesterov. "Preparation of Differentiated Recombinant Human β2-Microglobulin and Mouse β2-Microglobulin Proteins for its Detection in Class I HLA Chimeric Molecules". Journal Biomed 20, № 2 (2024): 21–31. http://dx.doi.org/10.33647/2074-5982-20-2-21-31.

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Transgenic humanized animals are increasingly in demand for biomedical research and pharmacological testing. More and more lines of transgenic animals are being created, including those with knockout of their own genes. There is an urgent need for an evidence base for the integration of a transgene, its expression, determination of the knockout state of its own gene at the molecular genetic level, detection of translation of the target protein in different organs and tissues, proof for the absence of protein synthesis (or its non-functionality), the gene of which has been modified. This requir
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15

Ureta-Vidal, Abel, Hüseyin Firat, Béatrice Pérarnau, and François A. Lemonnier. "Phenotypical and Functional Characterization of the CD8+ T Cell Repertoire of HLA-A2.1 Transgenic, H-2K b °D b ° Double Knockout Mice." Journal of Immunology 163, no. 5 (1999): 2555–60. http://dx.doi.org/10.4049/jimmunol.163.5.2555.

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Abstract Homozygous HLA-A2.1 transgenic H-2Kb°Db° double knockout (KO) mice were created. Their potential to develop HLA-A2.1-restricted cytolytic responses was compared with that of their classical transgenic counterparts, which still express H-2Kb, Db molecules. On cell surfaces, both strains express similar amounts of chimeric (α1α2 domains of human, α3 cytoplasmic domains of mouse) HLA-A2.1 molecules in noncovalent association with mouse β2-microglobulin. Compared with mice that are totally deprived of histocompatibility class Ia molecules (H-2Kb°Db° double KO), the expression of HLA-A2.1
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Nalawade, Saisha A., Niannian Ji, Ellen Kraig, and Thomas Forsthuber. "Aire is not essential for regulating autoimmune pathology in mice transgenic for human autoimmune-disease associated MHC class II genes HLA-DR2b and HLA-DR4." Journal of Immunology 200, no. 1_Supplement (2018): 167.8. http://dx.doi.org/10.4049/jimmunol.200.supp.167.8.

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Abstract The human MHC class II molecules HLA-DR2b (DRB1*1501) and HLA-DR4 (DRB1*0401) are strongly linked to increased susceptibility to autoimmune diseases, such as multiple sclerosis (MS) and rheumatoid arthritis (RA). However, their contribution to disease pathogenesis is not completely understood. Conceivably, autoimmune disease-associated HLA alleles could shape the repertoire of pathogenic T cells via central or peripheral tolerance. The ectopic expression of tissue-specific antigens promoted by the autoimmune regulator (AIRE) is thought to play a critical role in central tolerance. Air
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17

Santos, M., M. W. Schilham, L. H. Rademakers, J. J. Marx, M. de Sousa, and H. Clevers. "Defective iron homeostasis in beta 2-microglobulin knockout mice recapitulates hereditary hemochromatosis in man." Journal of Experimental Medicine 184, no. 5 (1996): 1975–85. http://dx.doi.org/10.1084/jem.184.5.1975.

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Previously, hepatic iron overload resembling that in hereditary hemachromatosis (HH) has been found in beta 2-microglobulin knockout (beta 2m-/-) mice. We have now characterized iron metabolism in beta 2m-/- mice. The mutant mice fail to limit the transfer of iron from mucosal cells into the plasma. Transferrin saturation is abnormally high. Pathologic iron depositions occur predominantly in liver parenchymal cells. Reconstitution with normal hematopoietic cells redistributes the iron from parenchymal to Kupffer cells, but does not correct the mucosal defect. We conclude that (a) iron metaboli
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Pascolo, Steve, Nathalie Bervas, Jan M. Ure, Austin G. Smith, François A. Lemonnier та Béatrice Pérarnau. "HLA-A2.1–restricted Education and Cytolytic Activity of CD8+ T Lymphocytes from β2 Microglobulin (β2m) HLA-A2.1 Monochain Transgenic H-2Db β2m Double Knockout Mice". Journal of Experimental Medicine 185, № 12 (1997): 2043–51. http://dx.doi.org/10.1084/jem.185.12.2043.

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Three different HLA-A2.1 monochains were engineered in which either the human or mouse β2-microglobulin (β2m) is covalently linked to the NH2 terminus of the heavy chain by a 15– amino acid long peptide: HHH, entirely human, HHD, with the mouse H-2Db α3, transmembrane, and cytoplasmic domains, and MHD, homologous to HHD but linked to the mouse β2mb. The cell surface expression and immunological capacities of the three monochains were compared with transfected cells, and the selected HHD construct was introduced by transgenesis in H-2Db−/− β2m−/− double knockout mice. Expression of this monocha
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Kushniarova, Lizaveta V., Alexandr A. Migas, Hanna V. Klych, Yauheni A. Lasiukov, and Alexander N. Meleshko. "Knockout of the T-cell receptor and HLA class I genes in human cells using the CRISPR /Cas9 system." Experimental Biology and Biotechnology, no. 2 (July 6, 2022): 19–26. http://dx.doi.org/10.33581/2957-5060-2022-2-19-26.

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The CRISPR /Cas9 system has found a wide application in cell biology as a tool for gene knockout. In particular, the CRISPR /Cas9 system is used to create allogeneic CAR-T lymphocytes by knocking out the genes TRAC, TRBC1, TRBC2 and B2M. To obtain a large number of cells of the desired phenotype, it is necessary to optimise the process of genomic editing, the effectiveness of which is determined by the sgRNA used. In this work, we experimentally determined the most effective sequences that allow to obtain up to 60.3 % of cells negative for the expression of the B2M protein and up to 71.8 % of
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Rajagopalan, Govindarajan, Ashenafi Tilahun, and Vaidehi Chowdhary. "Chronic activation with a staphylococcal superantigen drives the expansion of CD4, CD8 double negative T cells and promotes multiorgan inflammation mimicking systemic lupus erythematosus in HLA class II transgenic mice. (HUM7P.306)." Journal of Immunology 192, no. 1_Supplement (2014): 184.15. http://dx.doi.org/10.4049/jimmunol.192.supp.184.15.

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Abstract CD4 and CD8 coreceptors play an important role in the development and maturation of αβ TCR+ T cells. However, T cells lacking CD4 and CD8 (double negative T or DNT cells) are present in the periphery and are significantly expanded in systemic lupus erythematosus (SLE) and Sjogren’s syndrome. The antigens that cause expansion of these DNT cells are unknown. As T cell activation by superantigens does not require coreceptors, we hypothesized that superantigens could activate DNT cells and contribute to autoimmunity. HLA-DQ8 and HLA-DR3 transgenic mice lacking both CD4 and CD8 were genera
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Elliott, J. F., J. Liu, Z. N. Yuan, et al. "Autoimmune cardiomyopathy and heart block develop spontaneously in HLA-DQ8 transgenic IA knockout NOD mice." Proceedings of the National Academy of Sciences 100, no. 23 (2003): 13447–52. http://dx.doi.org/10.1073/pnas.2235552100.

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Chen, Liye, Hui Shi, Danai Koftori, et al. "Identification of an Unconventional Subpeptidome Bound to the Behçet's Disease-associated HLA-B*51:01 that is Regulated by Endoplasmic Reticulum Aminopeptidase 1 (ERAP1)." Molecular & Cellular Proteomics 19, no. 5 (2020): 871–83. http://dx.doi.org/10.1074/mcp.ra119.001617.

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Human leukocyte antigen (HLA) B*51:01 and endoplasmic reticulum aminopeptidase 1 (ERAP1) are strongly genetically associated with Behçet's disease (BD). Previous studies have defined two subgroups of HLA-B*51 peptidome containing proline (Pro) or alanine (Ala) at position 2 (P2). Little is known about the unconventional non-Pro/Ala2 HLA-B*51-bound peptides. We aimed to study the features of this novel subpeptidome, and investigate its regulation by ERAP1. CRISPR-Cas9 was used to generate an HLA-ABC-triple knockout HeLa cell line (HeLa.ABC-KO), which was subsequently transduced to express HLA-B
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Venkatasubramaniam, Arundhathi, Tulasikumari Kanipakala, Nader Ganjbaksh, et al. "A Critical Role for HlgA in Staphylococcus aureus Pathogenesis Revealed by A Switch in the SaeRS Two-Component Regulatory System." Toxins 10, no. 9 (2018): 377. http://dx.doi.org/10.3390/toxins10090377.

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Cytolytic pore-forming toxins including alpha hemolysin (Hla) and bicomponent leukotoxins play an important role in the pathogenesis of Staphylococcus aureus. These toxins kill the polymorphonuclear phagocytes (PMNs), disrupt epithelial and endothelial barriers, and lyse erythrocytes to provide iron for bacterial growth. The expression of these toxins is regulated by the two-component sensing systems Sae and Agr. Here, we report that a point mutation (L18P) in SaeS, the histidine kinase sensor of the Sae system, renders the S. aureus Newman hemolytic activity fully independent of Hla and drast
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Karkischenko, N. N., V. N. Lazarev, V. A. Manuvera, et al. "Principles of Creation of a Genetic Engineering Construction for Obtaining Humanized Transgenic Mice with <i>HLA-C*07:02:01:01</i>, as a Promote of Innovative Transgenic and Knockout Biomodels." Journal Biomed 20, no. 1 (2024): 8–20. http://dx.doi.org/10.33647/2074-5982-20-1-8-20.

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Genetic differences in different populations influence the mechanism and efficacy of drugs. Biomodels that take into account the peculiarities of genetic polymorphism in different individuals allow to more fully investigate the molecular-genetic mechanisms of action of pharmacological agents, including immunobiological ones. Recombinant DNA encoding a hybrid MHC class I protein containing human ß2-microglobulin fused with antigen-presenting domains (α1 and α2 domains) of the HLA-C*07:02:01:01 molecule and α3 domain of the mouse H2-complex was created. The purified linearized DNA fragment conta
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Chapoval, Svetlana P., Teresa Neeno, Christopher J. Krco, Eric V. Marietta, Jerry Harders, and Chella S. David. "HLA-DQ6 and HLA-DQ8 Transgenic Mice Respond to Ragweed Allergens and Recognize a Distinct Set of Epitopes on Short and Giant Ragweed Group 5 Antigens." Journal of Immunology 161, no. 4 (1998): 2032–37. http://dx.doi.org/10.4049/jimmunol.161.4.2032.

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Abstract We have investigated the genetic and molecular basis of immune responsiveness to short ragweed (SRW) (Ambrosia artemisiifolia) extract, and group 5 allergens from short and giant (Ambrosia trifida) ragweed using transgenic mice expressing DQ6 (HLA-DQA1*0103, HLA-DQB1*0601) and DQ8 (HLA-DQA1*0301, HLA-DQB1*0302) genes in class II knockout (Aβ0) mice. Panels of overlapping peptides spanning the Amb a 5 and Amb t 5 Ags were synthesized. Mice were immunized with whole SRW extract or individual peptides s.c. and lymph node cells (LNC) were challenged in vitro. Strong T cell responses to SR
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Catelli, Lucas Ferioli, Marcus Alexandre Finzi Corat, Nádia Ghinelli Amôr, et al. "Knockout of the Beta-2 Microglobulin Gene in Adipose Tissue-Derived Cells Using CRISPR/CAS9 System for the Generation of Universal HLA Class I Platelets." Blood 144, Supplement 1 (2024): 1266. https://doi.org/10.1182/blood-2024-205233.

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Platelet refractoriness is a recurring problem in the treatment of thrombocytopenic patients, hindering the restoration of normal circulating platelet levels after platelet transfusion therapy. The primary cause is the incompatibility between the transfused platelets' HLA Class I antigens and the patient's antibodies. The production of platelets in vitro from genetically edited stem cells may become a future source of HLA Class I universal platelets that could help mitigate this problem. Adipose tissue-derived mesenchymal stem/stromal cells line (ASCL), generated from the dedifferentiation of
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Dufva, Olli, Jay Klievink, Khalid Saeed, et al. "Genome-Scale CRISPR Screens Identify Essential Genes for Sensitivity to Natural Killer Cells in Hematological Malignancies." Blood 132, Supplement 1 (2018): 732. http://dx.doi.org/10.1182/blood-2018-99-117985.

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Abstract Immunotherapy is a promising approach to improve treatment responses in hematological malignancies. Accumulating evidence suggests a role for natural killer (NK) cells in controlling hematological malignancies. However, mechanisms regulating sensitivity or resistance of hematologic cancer cells to the effector function of NK cells are incompletely understood. Here, we performed genome-scale CRISPR-Cas9 loss-of-function screens to systematically map genes that regulate sensitivity of hematologic malignancies to NK cells. To screen for genes involved in the interaction between NK and ca
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Zaia, John A., Xiuli Li, Anne E. Franck, Xiwei Wu, Lia Thao, and Ghislaine Gallez-Hawkins. "Biologic and Immunologic Effects of Knockout of Human Cytomegalovirus pp65 Nuclear Localization Signal." Clinical and Vaccine Immunology 16, no. 6 (2009): 935–43. http://dx.doi.org/10.1128/cvi.00011-09.

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ABSTRACT The human cytomegalovirus (CMV) pp65 protein contains two bipartite nuclear localization signals (NLSs) at amino acids (aa) 415 to 438 and aa 537 to 561 near the carboxy terminus of CMV pp65 and a phosphate binding site related to kinase activity at lysine-436. A mutation of pp65 with K436N (CMV pp65mII) and further deletion of aa 537 to 561 resulted in a novel protein (pp65mIINLSKO, where NLSKO indicate NLS knockout) that is kinaseless and that has markedly reduced nuclear localization. The purpose of this study was to biologically characterize this protein and its immunogenicity com
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Chandrasekaran, Siddarth, Vignesh Janardhanam, Ian Cardle, et al. "A Layered Cloaking Strategy to Generate Allogeneic iPSC-Derived CD8 T-Cells That Evade NK Clearance." Blood 144, Supplement 1 (2024): 2045. https://doi.org/10.1182/blood-2024-210003.

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Gene-editing approaches have paved the way to manipulate allogeneic CAR-T cells for longer persistence by escaping host immune cell mediated rejection. While the design concepts for evading patient T-cell mediated rejection have been widely agreed upon, a lack of consensus remains around the optimal design for avoiding missing-self natural killer (NK) responses resulting from HLA Class I knockout. The most common approach for NK cell evasion includes knock in of HLA-E, a non-classical class I molecule with limited polymorphism that inhibits NK cells via binding to an inhibitory receptor NKG2A.
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Firat, H. "Comparative analysis of the CD8+ T cell repertoires of H-2 class I wild-type/HLA-A2.1 and H-2 class I knockout/HLA-A2.1 transgenic mice." International Immunology 14, no. 8 (2002): 925–34. http://dx.doi.org/10.1093/intimm/dxf056.

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Steinitz, Katharina N., Pauline M. van Helden, Brigitte Binder, et al. "CD4+ T-cell epitopes associated with antibody responses after intravenously and subcutaneously applied human FVIII in humanized hemophilic E17 HLA-DRB1*1501 mice." Blood 119, no. 17 (2012): 4073–82. http://dx.doi.org/10.1182/blood-2011-08-374645.

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Abstract Today it is generally accepted that B cells require cognate interactions with CD4+ T cells to develop high-affinity antibodies against proteins. CD4+ T cells recognize peptides (epitopes) presented by MHC class II molecules that are expressed on antigen-presenting cells. Structural features of both the MHC class II molecule and the peptide determine the specificity of CD4+ T cells that can bind to the MHC class II–peptide complex. We used a new humanized hemophilic mouse model to identify FVIII peptides presented by HLA-DRB1*1501. This model carries a knockout of all murine MHC class
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Rohrlich, P. S. "HLA-B*0702 transgenic, H-2KbDb double-knockout mice: phenotypical and functional characterization in response to influenza virus." International Immunology 15, no. 6 (2003): 765–72. http://dx.doi.org/10.1093/intimm/dxg073.

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Black, Kay E., Joseph A. Murray, and Chella S. David. "HLA-DQ Determines the Response to Exogenous Wheat Proteins: A Model of Gluten Sensitivity in Transgenic Knockout Mice." Journal of Immunology 169, no. 10 (2002): 5595–600. http://dx.doi.org/10.4049/jimmunol.169.10.5595.

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Guo, Chao, Yanying Fan, Alexander Aronov, et al. "113 CISH gene-knockout anti-CD70-CAR NK cells demonstrate potent anti-tumor activity against solid tumor cell lines and provide partial resistance to tumor microenvironment inhibition." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (2021): A123. http://dx.doi.org/10.1136/jitc-2021-sitc2021.113.

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BackgroundPeripheral blood natural killer (NK) cells are attractive candidates for adoptive cell therapy. NK cells possess innate ability for tumor cell killing and are also amenable to genomic engineering for enhanced functions. Moreover, NK cells possess an inherent capacity for allogeneic, off-the-shelf therapy since, unlike T cells, they are neither HLA-restricted nor known to cause graft-versus-host disease. Cytokine inducible SH2-containing protein (CISH) is a negative regulator of interleukin 15 (IL-15) signaling in natural killer (NK) cells. Here we show the potential application of CI
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Gu, Xiaorong, Songa Bae, Yahan Zhang, et al. "Loss of TET2 Increases MHC Class I Expression in Acute Myeloid Leukemia." Blood 144, Supplement 1 (2024): 4159. https://doi.org/10.1182/blood-2024-208348.

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Background: One of the major challenges in the treatment of acute myeloid leukemia (AML) is the elimination of undifferentiated immature blood cells, often referred to as leukemia stem and progenitor cells (LSPC). LSPCs persist after treatment and are considered a major cause of relapse and refractory disease. Despite initially high remission rates with recent advances in treatment strategies, relapse occurs in a large proportion of patients, leading to high mortality in AML. Myeloid neoplasia (MN) is driven by somatic mutations, with loss of function TET2 mutations (TET2MT) being one of the m
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Garner, Elizabeth, Erin Kelly, Sai Namburi, et al. "Abstract 3201: CB-012, an allogeneic anti-CLL-1 CAR-T cell therapy engineered with next-generation CRISPR technology to resist both the immunosuppressive tumor microenvironment and immune cell-mediated rejection, for patients with relapsed or refractory acute myeloid leukemia." Cancer Research 83, no. 7_Supplement (2023): 3201. http://dx.doi.org/10.1158/1538-7445.am2023-3201.

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Abstract Background: CB-012 is an allogeneic anti-CLL-1 CAR-T cell therapy in development for evaluation in relapsed or refractory acute myeloid leukemia (r/r AML). CB-012 is engineered with a next-generation CRISPR genome-editing technology to leverage both checkpoint disruption and immune cloaking to enhance persistence of CAR-T cell antitumor activity. Methods: Caribou’s CRISPR hybrid RNA-DNA (chRDNA) guides in combination with Cas12a were used to make five edits in the manufacture of CB-012. A fully human anti-CLL-1 CAR transgene was site-specifically inserted into the TRAC gene, thereby e
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Pajot, Anthony, Marie-Louise Michel, Nicolas Fazilleau, et al. "A mouse model of human adaptive immune functions:HLA-A2.1-/HLA-DR1-transgenicH-2 class I-/class II-knockout mice." European Journal of Immunology 34, no. 11 (2004): 3060–69. http://dx.doi.org/10.1002/eji.200425463.

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Dufva, Olli, Khalid Saeed, Sara Gandolfi, et al. "CRISPR Screens Identify Mechanisms of Natural Killer Cell Evasion across Blood Cancers." Blood 134, Supplement_1 (2019): 3597. http://dx.doi.org/10.1182/blood-2019-129837.

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Natural killer (NK) cells have been suggested to control progression and relapse in several hematological malignancies. Enhancing NK cell reactivity represents an attractive approach to improve treatment responses. However, mechanisms enabling evasion of hematologic cancer cells from NK cells are incompletely understood. To identify cancer cell-intrinsic factors enabling resistance to NK cell cytotoxicity, we conducted genome-wide CRISPR screens in a range of hematological malignancies. Cas9-expressing cancer cells from diverse hematological malignancies, including acute and chronic myeloid le
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Triolo, Taylor M., J. Quinn Matuschek, Roberto Castro-Gutierrez та ін. "Stem-Cell-Derived β-Like Cells with a Functional PTPN2 Knockout Display Increased Immunogenicity". Cells 11, № 23 (2022): 3845. http://dx.doi.org/10.3390/cells11233845.

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Type 1 diabetes is a polygenic disease that results in an autoimmune response directed against insulin-producing beta cells. PTPN2 is a known high-risk type 1 diabetes associated gene expressed in both immune- and pancreatic beta cells, but how genes affect the development of autoimmune diabetes is largely unknown. We employed CRISPR/Cas9 technology to generate a functional knockout of PTPN2 in human pluripotent stem cells (hPSC) followed by differentiating stem-cell-derived beta-like cells (sBC) and detailed phenotypical analyses. The differentiation efficiency of PTPN2 knockout (PTPN2 KO) sB
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Karkischenko, N. N., V. A. Ezerskiy, O. B. Zhukova, E. M. Koloskova та N. V. Petrova. "Increasing, the Specificity of Polyclonal Antibodies to Human and Mouse β2-Microglobulin as an Alternative to the Use of Monoclonal Antibodies in Immunological Analysis". Journal Biomed 20, № 2 (2024): 53–65. http://dx.doi.org/10.33647/2074-5982-20-2-53-65.

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Highly specific reagents, i.e., proteins and antibodies to them, are the necessary components of systems for verifying the effectiveness of transgenic/knockout animal biomodels. In particular, the identification of mouse and human β2-microglobulin in the protein fractions of organs and tissues of transgenic and β2m knockout mice of several HLA lines, which have been created in recent years at the Scientific Center of Biomedical Technologies of the FMBA of Russia, is the most important stage of their certification. At the first stage of our research, E. coli producing strains of recombinant mou
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Khare, Sanjay D., Michael J. Bull, Julie Hanson, Harvinder S. Luthra, and Chella S. David. "Spontaneous Inflammatory Disease in HLA-B27 Transgenic Mice Is Independent of MHC Class II Molecules: A Direct Role for B27 Heavy Chains and Not B27-Derived Peptides." Journal of Immunology 160, no. 1 (1998): 101–6. http://dx.doi.org/10.4049/jimmunol.160.1.101.

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Abstract Although association of HLA-B27 with human spondyloarthropathies has been known for several years, its role in disease pathogenesis is not understood. Recently, a few investigators have proposed that presentation of B27-derived peptides by MHC class II molecules may be the underlying mechanism. HLA-B27 transgenic rat and mouse models have provided a new tool for understanding the exact role of B27 in disease pathogenesis. HLA-B27 mice lacking endogenous β2-microglobulin (B27+β2mo) develop disease after they are transferred from the barrier facility to the conventional colony. This mod
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Crivello, Pietro, Müberra Ahci, Fabienne Maaßen та ін. "Multiple Knockout of Classical HLA Class II β-Chains by CRISPR/Cas9 Genome Editing Driven by a Single Guide RNA". Journal of Immunology 202, № 6 (2019): 1895–903. http://dx.doi.org/10.4049/jimmunol.1800257.

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Robinson, Philip C., Eugene Lau, Patricia Keith, et al. "ERAP2functional knockout in humans does not alter surface heavy chains or HLA-B27, inflammatory cytokines or endoplasmic reticulum stress markers." Annals of the Rheumatic Diseases 74, no. 11 (2015): 2092–95. http://dx.doi.org/10.1136/annrheumdis-2015-207467.

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Firat, Hüseyin, Francisco Garcia-Pons, Sophie Tourdot, et al. "H-2 class I knockout, HLA-A2.1-transgenic mice: a versatile animal model for preclinical evaluation of antitumor immunotherapeutic strategies." European Journal of Immunology 29, no. 10 (1999): 3112–21. http://dx.doi.org/10.1002/(sici)1521-4141(199910)29:10<3112::aid-immu3112>3.0.co;2-q.

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Yang, Hongyun, Wen Jiang, Emma E. Furth, et al. "Intestinal inflammation reduces expression of DRA, a transporter responsible for congenital chloride diarrhea." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 6 (1998): G1445—G1453. http://dx.doi.org/10.1152/ajpgi.1998.275.6.g1445.

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The pathogenesis of diarrhea in intestinal inflammatory states is a multifactorial process involving the effects of inflammatory mediators on epithelial transport function. The effect of colonic inflammation on the gene expression of DRA (downregulated in adenoma), a chloride-sulfate anion transporter that is mutated in patients with congenital chloridorrhea, was examined in vivo as well as in an intestinal epithelial cell line. DRA mRNA expression was diminished five- to sevenfold in the HLA-B27/β2m transgenic rat compared with control. In situ hybridization showed that DRA, which is normally
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Hahn, Cynthia K., Gavin E. Hooper, Alexandra Forman, et al. "SEC62 Regulates HLA-E Expression in Diffuse Large B-Cell Lymphoma to Function As a Mechanism of Immune Evasion." Blood 144, Supplement 1 (2024): 335. https://doi.org/10.1182/blood-2024-210613.

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The expression of HLA-E, a non-classical HLA class I molecule, is an emerging mechanism of immune escape in cancer. Increased HLA-E is associated with poor prognosis in multiple malignancies and is a mechanism of resistance to immune-based therapies via an inhibitory interaction with the NKG2A/CD94 receptor on NK and T cells. We identified high expression of HLA-E in diffuse large B-cell lymphoma (DLBCL) and hypothesized that this may constitute an immune evasion mechanism that could be therapeutically targetable in this disease. We found that DLBCL has the highest median gene expression of HL
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Moise, Leonard, Jonathan Skupsky, Ryan Tassone, et al. "De-Immunization of Human Factor VIII: Identification of Epitopes in the C2 Domain." Blood 112, no. 11 (2008): 1030. http://dx.doi.org/10.1182/blood.v112.11.1030.1030.

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Abstract Most immune responses to protein antigens are dependent on T-cell recognition of discrete peptide epitopes presented in an MHC groove. The pattern of peptide recognition can be predicted from the primary structure of a given protein based on residues that bind (anchor) to a given HLA phenotype. Algorithms such as EpiMatrix can be applied to identify such epitopes and measure the potential immunogenicity of proteins based on epitope content. One approach to reduce immunogenicity is to generate recombinant proteins whose constituent epitopes have been modified so as to reduce their HLA
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Song, Nianbin, Yuri Poluektov, Robin Welsh, and Scheherazade Sadegh-Nasseri. "MHC class II antigen-processing chaperone H2-O shapes CD4 T cell receptor repertoire." Journal of Immunology 196, no. 1_Supplement (2016): 46.11. http://dx.doi.org/10.4049/jimmunol.196.supp.46.11.

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Abstract HLA-DO (DO) is a MHC class II-encoded, nonpolymorphic heterodimeric protein in humans (known as H2-O in mice). It is expressed only in thymic medulla, B lymphocytes and some subsets of dendritic cells. Although DO is found to form a stable complex with HLA—DM (DM), its physical function remains unknown. Some studies have shown that it inhibits the activity of DM to edit peptide presentation on MHC II molecules while others reported that the DO can up- or downmodulate presentation of certain peptides in association with DM on HLA-DR4 molecules. To solve this controversy, our lab recent
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Chen, Huanhuan, Keqing Yang, Lingxiao Pang, Jing Fei, Yongliang Zhu, and Jianwei Zhou. "ANKRD22 is a potential novel target for reversing the immunosuppressive effects of PMN-MDSCs in ovarian cancer." Journal for ImmunoTherapy of Cancer 11, no. 2 (2023): e005527. http://dx.doi.org/10.1136/jitc-2022-005527.

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BackgroundOvarian cancer is the deadliest type of malignant gynecological tumor. Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) are involved ovarian cancer and are closely related to adverse outcomes. However, the immunosuppressive mechanism of PMN-MDSCs remains elusive.MethodsThe types and numbers of ANKRD22-expressing cells were investigated by bioinformatics analysis and immunohistochemical staining.Ankrd22-/-C57BL/6 mice were constructed with CRISPR-Cas9 technology. Mouse PMN-MDSCs were obtained from bone marrow (BM)-derived CD11b+Ly6G+Ly6Clowcells sorted by fluorescence-ac
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Liu, Fuguo, Mubin Tarannum, Yingjie Zhao, et al. "One-Step Construction of Allogeneic CAR-NK Cells Preventing Rejection and Mediating Enhanced Anti-Tumor Responses." Blood 144, Supplement 1 (2024): 915. https://doi.org/10.1182/blood-2024-198167.

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Chimeric antigen receptor (CAR)-armed immune cells have demonstrated promising efficacy in several hematologic malignancies. There is a great interest in developing allogeneic “off-the-shelf” cellular therapies to reduce manufacturing time and costs, allow multiple dosing, and increase accessibility. To mitigate the problem of rejection of allogeneic products, common approaches include abrogation of MHC I expression by deleting b2-microglobulin (B2M) or TAP genes to prevent host T cell killing, and expression of HLA-E, HLA-G or CD47 to inhibit host NK killing. Typically, B2M or TAP knockout is
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