烟酰胺代谢通过推定的 HS1BP3-SIRT1-FOXO3-BCL6 轴限制记忆 CD8⁺ T 细胞形成
Nicotinamide Metabolism Constrains Memory CD8(+) T Cell Formation Through a Putative HS1BP3-SIRT1-FOXO3-BCL6 Axis.
我们的研究结果确定了HS1BP3是CD8+ T细胞记忆的调节因子,并表明其效应与烟酰胺代谢及SIRT1-FOXO3-BCL6信号轴的改变有关。
FRONTIER PAPERS
Nicotinamide Metabolism Constrains Memory CD8(+) T Cell Formation Through a Putative HS1BP3-SIRT1-FOXO3-BCL6 Axis.
我们的研究结果确定了HS1BP3是CD8+ T细胞记忆的调节因子,并表明其效应与烟酰胺代谢及SIRT1-FOXO3-BCL6信号轴的改变有关。
Intrinsic tumor cell line immunogenicity may drive CAR-independent T cell responses and confound CAR T cell preclinical modeling.
这些发现表明,某些肿瘤细胞系能够引发强烈的同种异体T细胞反应,且不依赖于CAR特异性,揭示了常用临床前模型的一个重要局限性,并凸显了CAR T细胞疗效评估中出现假阳性的可能性。
Engineering Interferon-γ-Enhanced Chimeric Antigen Receptor Macrophages via Lipid-Assisted Polymeric Nanoparticles for Cancer Immunotherapy.
目的 To develop an efficient strategy for in vivo engineering of M1-like CAR-Ms for cancer therapy. 方法 We designed a lentiviral vector encoding a CAR targeting BCMA and a cytokine cassette. Macrophages were transduced and
A guide to CAR T cell therapies: development, current status and future prospects.
自 2017 年首次获得临床批准以来,嵌合抗原受体(CAR)T 细胞疗法已成为重定向免疫应答以对抗癌症的最有力手段之一。
Pivotal role of PD-1/PD-L1 as an immune checkpoint in lymphoma and solid tumor: Cellular organization, clinical implications & the potential of small
肿瘤免疫治疗已成为晚期恶性肿瘤治疗的范式转变。
Redirecting Cholesterol Metabolism During Ex Vivo Biomanufacturing Enhances the Metabolic Fitness and Antitumor Efficacy of CAR-T Cells.
CAR-T 细胞疗法彻底改变了血液系统恶性肿瘤的治疗;然而,其在实体瘤中的疗效仍有限,部分原因是体外制备过程中的 T 细胞耗竭。
Clickable Universal Tumor-Antigen Equipping Strategy for Remedial Chimeric Antigen Receptor T Cells to Destroy Solid Tumors.
嵌合抗原受体(CAR)-T细胞疗法在白血病和淋巴瘤中展现出显著疗效,但实体瘤仍大多难以治疗,原因在于肿瘤特异性抗原稀缺及广泛的抗原异质性,加之CAR-T细胞快速耗竭限制了其功能与持久性。
Spectrum, pathobiology, mechanistic insights and diagnostic challenges of post-CAR T cell therapy lymphoproliferative disorders.
嵌合抗原受体(CAR)T细胞疗法现已广泛用于治疗各种血液系统恶性肿瘤,并在实体瘤和自身免疫性疾病中的应用日益增多。
Timosaponin AIII enhances CAR-T cell potency and prevents relapse through impairing CAR-Tregs.
嵌合抗原受体(CAR)-T 细胞疗法已改变了复发/难治性 DLBCL 的治疗,但由调节性 T 细胞(Tregs)驱动的耐药限制了其疗效。
Metabolic activation using fructose-1,6-bisphosphate microparticles of non-virally LNP-generated CAR-macrophages induces anti-tumor immune responses.
尽管嵌合抗原受体(CAR)-T细胞疗法在血液系统恶性肿瘤中已显示出显著的临床疗效,但其对实体瘤的作用仍然有限,这在很大程度上是由于T细胞向肿瘤微环境(TME)的浸润不足所致。
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