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Relevant bibliographies by topics / HLA knockout

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Journal articles

Academic literature on the topic 'HLA knockout'

Author: Grafiati

Published: 12 April 2025

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Journal articles on the topic "HLA knockout"

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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