搜索结果: 'gmp t cell activator'

Shirato K et al. ( 2017) Virology November 0--1

Wild-type human coronaviruses prefer cell-surface TMPRSS2 to endosomal cathepsins for cell entry

Human coronaviruses (HCoVs) enter cells via two distinct pathways: the endosomal pathway using cathepsins to activate spike protein and the cell-surface or early endosome pathway using extracellular proteases such as transmembrane protease serine 2 (TMPRSS2). We previously reported that clinical isolates of HCoV-229E preferred cell-surface TMPRSS2 to endosomal cathepsin for cell entry,and that they acquired the ability to use cathepsin L by repeated passage in cultured cells and were then able to enter cells via the endosomal pathway. Here,we show that clinical isolates of HCoV-OC43 and -HKU1 preferred the cell-surface TMRRSS2 to endosomal cathepsins for cell entry,similar to HCoV-229E. In addition,the cell-culture-adapted HCoV-OC43 lost the ability to infect and replicate in air-liquid interface cultures of human bronchial tracheal epithelial cells. These results suggest that circulating HCoVs in the field generally use cell-surface TMPRSS2 for cell entry,not endosomal cathepsins,in human airway epithelial cells. View Publication

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05008

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PneumaCult™-ALI 培养基

PneumaCult™-ALI 培养基含12 mm Transwell®插件

PneumaCult™-ALI 培养基含6.5 mm Transwell®插件

PneumaCult™-Ex 培养基

Improving Reproducibility of Your hPSC Research by Generating a High-Quality Cell Bank

21:53

线上讲座

Improving Reproducibility of Your hPSC Research by Generating a High-Quality Cell Bank

发布日期: 05/27/2020

(Feb 2025) Nature Communications 16

Metabolic deficiencies underlie reduced plasmacytoid dendritic cell IFN-I production following viral infection

Type I Interferons (IFN-I) are central to host protection against viral infections,with plasmacytoid dendritic cells (pDC) being the most significant source,yet pDCs lose their IFN-I production capacity following an initial burst of IFN-I,resulting in susceptibility to secondary infections. The underlying mechanisms of these dynamics are not well understood. Here we find that viral infection reduces the capacity of pDCs to engage both oxidative and glycolytic metabolism. Mechanistically,we identify lactate dehydrogenase B (LDHB) as a positive regulator of pDC IFN-I production in mice and humans; meanwhile,LDHB deficiency is associated with suppressed IFN-I production,pDC metabolic capacity,and viral control following infection. In addition,preservation of LDHB expression is sufficient to partially retain the function of otherwise exhausted pDCs,both in vitro and in vivo. Furthermore,restoring LDHB in vivo in pDCs from infected mice increases IFNAR-dependent,infection-associated pathology. Our work thus identifies a mechanism for balancing immunity and pathology during viral infections,while also providing insight into the highly preserved infection-driven pDC inhibition. Plasmacytoid dendritic cells (pDC) are the major IFN-I-producing cells,but this production returns to baseline soon after viral infection. Here the authors show that this decrease in IFN-I production and related pDC functions may be attributed to suppressed oxidative and glycolytic metabolism of pDCs,with lactate dehydrogenase B identified as a regulator. View Publication

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19860

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19860RF

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EasySep™小鼠Streptavidin RapidSpheres™分选试剂盒

EasySep™人浆细胞样DC富集试剂盒

RoboSep™ 人浆细胞样DC富集试剂盒含滤芯吸头

RoboSep™ 小鼠Streptavidin RapidSpheres™分选试剂盒

M. Zhu et al. (Dec 2025) Nature Communications 16

Targeting leukemic stem cell biomechanics suppresses stemness and enhances NK cell-mediated immunotherapy

Acute myeloid leukemia (AML) is primarily driven by leukemic stem cells (LSCs),the main cause of relapse and therapy resistance. Here,we discover that LSCs are predominantly small and mechanically soft. These mechanical properties enable their selective isolation using microfluidic chips. Single-cell RNA-sequencing of primary human AML bone marrow identifies enrichment of LSCs within the FSClow ALDH1A1+ subpopulation,which exhibits long-term stemness in functional assays. Notably,inhibiting ALDH1A1 in these cells promotes F-actin polymerization and increases cellular stiffness,reducing their stemness while enhancing their susceptibility to natural killer (NK) cell-mediated cytotoxicity. In AML patient-derived xenograft models,the combination of ALDH1A1 inhibition with NK cell therapy markedly suppresses leukemia progression. These findings suggest that targeting the mechanical properties of LSC offers a promising strategy to overcome AML treatment resistance,providing insights into stem cell mechanobiology and paving the way for combining targeted therapies with immunotherapy to improve clinical outcomes. Leukemic stem cells (LSCs) drive relapse and therapy resistance in acute myeloid leukemia (AML). Here,the authors show that increasing the stiffness of LSCs reduces their stemness and enhances their susceptibility to natural killer cell-mediated immunotherapy in AML. View Publication

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01700

09600

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ALDEFLUOR™ 试剂盒

StemSpan™ SFEM

新闻

BC Children’s Hospital Announces First of Its Kind Stem Cell Research Technology

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发布日期: 04/28/2022

Nature Research Round Table: Regulations Around Human Induced Pluripotent Stem Cell Registration

21:35

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Nature Research Round Table: Regulations Around Human Induced Pluripotent Stem Cell Registration

发布日期: 11/01/2019

科学海报

Easy 250 EasySep™ Magnet: A Novel Magnetic Platform for Large-Volume Cell Isolation

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ISSCR Standards in Action: Advancements in Cell Line Generation and Organoid Innovation

24:25

线上讲座

ISSCR Standards in Action: Advancements in Cell Line Generation and Organoid Innovation

发布日期: 08/01/2024

Quality by Design: Reagents and Support for hPSC-Derived Cell and Gene Therapies

39:33

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Quality by Design: Reagents and Support for hPSC-Derived Cell and Gene Therapies

发布日期: 08/16/2021

抗人CD69（AIM）抗体，clone FN50 抗人CD69小鼠Monoclonal 抗体

重组人干扰素γ 干扰素-γ

重组人MCP-1 （CCL2） 单核细胞趋化蛋白1

搜索结果: 'gmp t cell activator'

Wild-type human coronaviruses prefer cell-surface TMPRSS2 to endosomal cathepsins for cell entry

Metabolic deficiencies underlie reduced plasmacytoid dendritic cell IFN-I production following viral infection

Targeting leukemic stem cell biomechanics suppresses stemness and enhances NK cell-mediated immunotherapy

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