Product Information
Items 1429 to 1440 of 13914 total
- Reference(Jun 2024) Nature Immunology 25 8
A humanized mouse that mounts mature class-switched, hypermutated and neutralizing antibody responses
Humanized mice are limited in terms of modeling human immunity, particularly with regards to antibody responses. Here we constructed a humanized (THX) mouse by grafting non-γ-irradiated, genetically myeloablated KitW-41J mutant immunodeficient pups with human cord blood CD34+ cells, followed by 17β-estradiol conditioning to promote immune cell differentiation. THX mice reconstitute a human lymphoid and myeloid immune system, including marginal zone B cells, germinal center B cells, follicular helper T cells and neutrophils, and develop well-formed lymph nodes and intestinal lymphoid tissue, including Peyer’s patches, and human thymic epithelial cells. These mice have diverse human B cell and T cell antigen receptor repertoires and can mount mature T cell-dependent and T cell-independent antibody responses, entailing somatic hypermutation, class-switch recombination, and plasma cell and memory B cell differentiation. Upon flagellin or a Pfizer-BioNTech coronavirus disease 2019 (COVID-19) mRNA vaccination, THX mice mount neutralizing antibody responses to Salmonella or severe acute respiratory syndrome coronavirus 2 Spike S1 receptor-binding domain, with blood incretion of human cytokines, including APRIL, BAFF, TGF-β, IL-4 and IFN-γ, all at physiological levels. These mice can also develop lupus autoimmunity after pristane injection. By leveraging estrogen activity to support human immune cell differentiation and maturation of antibody responses, THX mice provide a platform to study the human immune system and to develop human vaccines and therapeutics. Humanized mice have been a valuable tool for modeling human immunology but are limited in their ability to model human antibody responses. Here the authors present their THX humanized mouse that does model human antibody responses and test its suitability for vaccination and autoimmunity studies.Catalog #: Product Name: 17856 EasySep™ Human CD34 Positive Selection Kit II Catalog #: 17856 Product Name: EasySep™ Human CD34 Positive Selection Kit II Reference(Jul 2024) Frontiers in Immunology 15Single cell multi-omic analysis identifies key genes differentially expressed in innate lymphoid cells from COVID-19 patients
IntroductionInnate lymphoid cells (ILCs) are enriched at mucosal surfaces where they respond rapidly to environmental stimuli and contribute to both tissue inflammation and healing. MethodsTo gain insight into the role of ILCs in the pathology and recovery from COVID-19 infection, we employed a multi-omics approach consisting of Abseq and targeted mRNA sequencing to respectively probe the surface marker expression, transcriptional profile and heterogeneity of ILCs in peripheral blood of patients with COVID-19 compared with healthy controls. ResultsWe found that the frequency of ILC1 and ILC2 cells was significantly increased in COVID-19 patients. Moreover, all ILC subsets displayed a significantly higher frequency of CD69-expressing cells, indicating a heightened state of activation. ILC2s from COVID-19 patients had the highest number of significantly differentially expressed (DE) genes. The most notable genes DE in COVID-19 vs healthy participants included a) genes associated with responses to virus infections and b) genes that support ILC self-proliferation, activation and homeostasis. In addition, differential gene regulatory network analysis revealed ILC-specific regulons and their interactions driving the differential gene expression in each ILC. DiscussionOverall, this study provides mechanistic insights into the characteristics of ILC subsets activated during COVID-19 infection.Catalog #: Product Name: 17975 EasySepâ„¢ Human Pan-ILC Enrichment Kit Catalog #: 17975 Product Name: EasySepâ„¢ Human Pan-ILC Enrichment Kit Reference(Jul 2024) Scientific Reports 14Identification of organs of origin of macrophages that produce presepsin via neutrophil extracellular trap phagocytosis
Presepsin (P-SEP) is a specific biomarker for sepsis. Monocytes produce P-SEP by phagocytosing neutrophil extracellular traps (NETs). Herein, we investigated whether M1 macrophages (M1 MΦs) are the primary producers of P-SEP after NET phagocytosis. We co-cultured M1 MΦs and NETs from healthy participants, measured P-SEP levels in the culture medium supernatant, and detected P-SEP using western blotting. When NETs were co-cultured with M1 MΦs, the P-SEP level of the culture supernatant was high. Notably, we demonstrated, for the first time, the intracellular kinetics of P-SEP production by M1 MΦs via NET phagocytosis: M1 MΦs produced P-SEP intracellularly 15 min after NET phagocytosis and then released it extracellularly. In a sepsis mouse model, the blood NET ratio and P-SEP levels, detected using ELISA, were significantly increased (p < 0.0001). Intracellular P-SEP analysis via flow cytometry demonstrated that lung, liver, and kidney MΦs produced large amounts of P-SEP. Therefore, we identified these organs as the origin of M1 MΦs that produce P-SEP during sepsis. Our data indicate that the P-SEP level reflects the trend of NETs, suggesting that monitoring P-SEP can be used to both assess NET-induced organ damage in the lungs, liver, and kidneys during sepsis and determine treatment efficacy.Catalog #: Product Name: 19359 EasySep™ Human Monocyte Isolation Kit Catalog #: 19359 Product Name: EasySep™ Human Monocyte Isolation Kit Reference(Jul 2024) Frontiers in Pharmacology 15 1Pharmacologic inhibition of dipeptidyl peptidase 1 (cathepsin C) does not block
Recently developed small-molecule inhibitors of the lysosomal protease dipeptidyl peptidase 1 (DPP1), also known as cathepsin C (CatC), can suppress suppurative inflammation in vivo by blocking the processing of zymogenic (pro-) forms of neutrophil serine proteases (NSPs), including neutrophil elastase, proteinase 3, and cathepsin G. DPP1 also plays an important role in activating granzyme serine proteases that are expressed by cytotoxic T lymphocytes (CTL) and natural killer (NK) cells. Therefore, it is critical to determine whether DPP1 inhibition can also cause off-target suppression of CTL/NK-cell-mediated killing of virus-infected or malignant cells. Herein, we demonstrate that the processing of human granzymes A and B, transitioning from zymogen to active proteases, is not solely dependent on DPP1. Thus, the killing of target cells by primary human CD8+ T cells, NK cells, and gene-engineered anti-CD19 CAR T cells was not blocked in vitro even after prior exposure to high concentrations of the reversible DPP1 inhibitor brensocatib. Consistent with this observation, the turnover of model granzyme A/B peptide substrates in the human CTL/NK cell lysates was not significantly reduced by brensocatib. In contrast, preincubation with brensocatib almost entirely abolished (>90%) both the cytotoxic activity of mouse CD8+ T cells and granzyme substrate turnover. Overall, our finding that the effects of DPP1 inhibition on human cytotoxic lymphocytes are attenuated in comparison to those of mice indicates that granzyme processing/activation pathways differ between mice and humans. Moreover, the in vitro data suggest that human subjects treated with reversible DPP1 inhibitors, such as brensocatib, are unlikely to experience any appreciable deficits in CTL/NK-cell-mediated immunities.Catalog #: Product Name: 10970 ImmunoCultâ„¢ Human CD3/CD28/CD2 T Cell Activator 17951 EasySepâ„¢ Human T Cell Isolation Kit 100-0785 ImmunoCultâ„¢ Human CD3/CD28/CD2 T Cell Activator Catalog #: 10970 Product Name: ImmunoCultâ„¢ Human CD3/CD28/CD2 T Cell Activator Catalog #: 17951 Product Name: EasySepâ„¢ Human T Cell Isolation Kit Catalog #: 100-0785 Product Name: ImmunoCultâ„¢ Human CD3/CD28/CD2 T Cell Activator Reference(Jul 2024) Nature Cell Biology 26 7Neutrophil-derived migrasomes are an essential part of the coagulation system
Migrasomes are organelles that are generated by migrating cells. Here we report the key role of neutrophil-derived migrasomes in haemostasis. We found that a large number of neutrophil-derived migrasomes exist in the blood of mice and humans. Compared with neutrophil cell bodies and platelets, these migrasomes adsorb and enrich coagulation factors on the surface. Moreover, they are highly enriched with adhesion molecules, which enable them to preferentially accumulate at sites of injury, where they trigger platelet activation and clot formation. Depletion of neutrophils, or genetic reduction of the number of these migrasomes, significantly decreases platelet plug formation and impairs coagulation. These defects can be rescued by intravenous injection of purified neutrophil-derived migrasomes. Our study reveals neutrophil-derived migrasomes as a previously unrecognized essential component of the haemostasis system, which may shed light on the cause of various coagulation disorders and open therapeutic possibilities. Jiang et al. document an abundance of neutrophil-derived migrasomes in the blood of mice and humans and show that migrasomes are enriched in coagulation factors, accumulate at sites of injury and trigger platelet activation and clot formation.Catalog #: Product Name: 19762 EasySepâ„¢ Mouse Neutrophil Enrichment Kit 17957 EasySepâ„¢ Human Neutrophil Isolation Kit Catalog #: 19762 Product Name: EasySepâ„¢ Mouse Neutrophil Enrichment Kit Catalog #: 17957 Product Name: EasySepâ„¢ Human Neutrophil Isolation Kit Reference(May 2024) iScience 27 7Metabolic reprogramming and dysregulated IL-17 production impairs CD4 TÂ cell function post sepsis
SummarySepsis survivors are at high risk for infection-related rehospitalization and mortality for years following the resolution of the acute septic event. These infection-causing microorganisms generally do not cause disease in immunocompetent hosts, suggesting that the post-septic immune response is compromised. Given the importance of CD4 T cells in the development of long-lasting protective immunity, we analyzed their post-septic function. Here we showed that sepsis induced chronic increased and non-specific production of IL-17 by CD4 T cells, resulting in the inability to mount an effective immune response to a secondary pneumonia challenge. Altered cell function was associated with metabolic reprogramming, characterized by mitochondrial dysfunction and increased glycolysis. This metabolic reprogramming began during the acute septic event and persisted long after sepsis had resolved. Our findings reveal cell metabolism as a potential therapeutic target. Given the critical role of cell metabolism in the physiological and pathophysiological processes of immune cells, these findings reveal a potential new therapeutic target to help mitigate sepsis survivors’ susceptibility to secondary infections. Graphical abstract Highlights•Sepsis survivors demonstrate dysfunctional CD4 T cell immunity•Sepsis induces persistent mitochondrial dysfunction in CD4 T cells•Post-septic CD4 T cells are highly glycolytic and exhibit a Th17 phenotype•Sepsis impairs the CD4 T cell recall response Physiology; Molecular biology; Immunology; Components of the immune systemCatalog #: Product Name: 19852 EasySepâ„¢ Mouse CD4+ T Cell Isolation Kit Catalog #: 19852 Product Name: EasySepâ„¢ Mouse CD4+ T Cell Isolation Kit Safety Data SheetCatalog #: Product Name: 100-1097 ³§³Ù±ð³¾³§±è²¹²Ôâ„¢-´¡°¿¹ó Catalog #: 100-1097 Product Name: ³§³Ù±ð³¾³§±è²¹²Ôâ„¢-´¡°¿¹ó Reference(Jul 2024) Nature Communications 15Tumor cell-directed STING agonist antibody-drug conjugates induce type III interferons and anti-tumor innate immune responses
Activating interferon responses with STING agonists (STINGa) is a current cancer immunotherapy strategy, and therapeutic modalities that enable tumor-targeted delivery via systemic administration could be beneficial. Here we demonstrate that tumor cell-directed STING agonist antibody-drug-conjugates (STINGa ADCs) activate STING in tumor cells and myeloid cells and induce anti-tumor innate immune responses in in vitro, in vivo (in female mice), and ex vivo tumor models. We show that the tumor cell-directed STINGa ADCs are internalized into myeloid cells by Fcγ-receptor-I in a tumor antigen-dependent manner. Systemic administration of STINGa ADCs in mice leads to STING activation in tumors, with increased anti-tumor activity and reduced serum cytokine elevations compared to a free STING agonist. Furthermore, STINGa ADCs induce type III interferons, which contribute to the anti-tumor activity by upregulating type I interferon and other key chemokines/cytokines. These findings reveal an important role for type III interferons in the anti-tumor activity elicited by STING agonism and provide rationale for the clinical development of tumor cell-directed STINGa ADCs. Activation of the STING pathway can promote anti-tumor immunity. Here the authors generate tumor cell-directed STING agonist antibody-drug conjugates that activate STING in tumor and myeloid cells, promoting anti-tumor innate immune responses in preclinical cancer models.Catalog #: Product Name: 17858 EasySep™ Human CD14 Positive Selection Kit II Catalog #: 17858 Product Name: EasySep™ Human CD14 Positive Selection Kit II Reference(Jun 2024) bioRxiv 37NRF2-dependent regulation of the prostacyclin receptor PTGIR drives CD8 T cell exhaustion
The progressive decline of CD8 T cell effector function—also known as terminal exhaustion—is a major contributor to immune evasion in cancer. Yet, the molecular mechanisms that drive CD8 T cell dysfunction remain poorly understood. Here, we report that the Kelch-like ECH-associated protein 1 (KEAP1)-Nuclear factor erythroid 2-related factor 2 (NRF2) signaling axis, which mediates cellular adaptations to oxidative stress, directly regulates CD8 T cell exhaustion. Transcriptional profiling of dysfunctional CD8 T cells from chronic infection and cancer reveals enrichment of NRF2 activity in terminally exhausted (Texterm) CD8 T cells. Increasing NRF2 activity in CD8 T cells (via conditional deletion of KEAP1) promotes increased glutathione production and antioxidant defense yet accelerates the development of terminally exhausted (PD-1+TIM-3+) CD8 T cells in response to chronic infection or tumor challenge. Mechanistically, we identify PTGIR, a receptor for the circulating eicosanoid prostacyclin, as an NRF2-regulated protein that promotes CD8 T cell dysfunction. Silencing PTGIR expression restores the anti-tumor function of KEAP1-deficient T cells. Moreover, lowering PTGIR expression in CD8 T cells both reduces terminal exhaustion and enhances T cell effector responses (i.e. IFN-γ and granzyme production) to chronic infection and cancer. Together, these results establish the KEAP1-NRF2 axis as a metabolic sensor linking oxidative stress to CD8 T cell dysfunction and identify the prostacyclin receptor PTGIR as an NRF2-regulated immune checkpoint that regulates CD8 T cell fate decisions between effector and exhausted states. One Sentence Summary:The KEAP1-NRF2 pathway is hyperactivated in terminally exhausted CD8 T cells and drives T cell dysfunction via transcriptional regulation of the prostacyclin receptor, Ptgir.Catalog #: Product Name: 19853 EasySep™ Mouse CD8+ T Cell Isolation Kit 17667 EasySep™ Mouse APC Positive Selection Kit II Catalog #: 19853 Product Name: EasySep™ Mouse CD8+ T Cell Isolation Kit Catalog #: 17667 Product Name: EasySep™ Mouse APC Positive Selection Kit II Reference(Jun 2024) Cell Reports Medicine 5 6A CD36-dependent non-canonical lipid metabolism program promotes immune escape and resistance to hypomethylating agent therapy in AML
SummaryEnvironmental lipids are essential for fueling tumor energetics, but whether these exogenous lipids transported into cancer cells facilitate immune escape remains unclear. Here, we find that CD36, a transporter for exogenous lipids, promotes acute myeloid leukemia (AML) immune evasion. We show that, separately from its established role in lipid oxidation, CD36 on AML cells senses oxidized low-density lipoprotein (OxLDL) to prime the TLR4-LYN-MYD88-nuclear factor κB (NF-κB) pathway, and exogenous palmitate transfer via CD36 further potentiates this innate immune pathway by supporting ZDHHC6-mediated MYD88 palmitoylation. Subsequently, NF-κB drives the expression of immunosuppressive genes that inhibit anti-tumor T cell responses. Notably, high-fat-diet or hypomethylating agent decitabine treatment boosts the immunosuppressive potential of AML cells by hijacking CD36-dependent innate immune signaling, leading to a dampened therapeutic effect. This work is of translational interest because lipid restriction by US Food and Drug Administration (FDA)-approved lipid-lowering statin drugs improves the efficacy of decitabine therapy by weakening leukemic CD36-mediated immunosuppression. Graphical abstract Highlights•CD36 on AML cells suppresses T cell proliferation independently of lipid oxidation•OxLDL and palmitate synergize to inhibit T cell activity via CD36 signaling in AML cells•Targeting CD36 signaling with statins improves the efficacy of decitabine therapy in AML Guo et al. find that OxLDL and palmitate uptake by AML cells synergistically upregulates CD36-mediated innate immune signaling to suppress T cell activity. High-fat-diet or decitabine treatment dampened the therapeutic effect by hijacking CD36 signaling. Targeting the CD36 immunosuppressive pathway with statins improves the efficacy of decitabine therapy in AML.Catalog #: Product Name: 09600 StemSpan™ SFEM 09605 StemSpan™ SFEM II 17897 EasySep™ Human Cord Blood CD34 Positive Selection Kit III Catalog #: 09600 Product Name: StemSpan™ SFEM Catalog #: 09605 Product Name: StemSpan™ SFEM II Catalog #: 17897 Product Name: EasySep™ Human Cord Blood CD34 Positive Selection Kit III Reference(May 2024) Molecular cell 84 11Pathways for macrophage uptake of cell-free circular RNAs
SUMMARY Circular RNAs (circRNAs) are stable RNAs present in cell-free RNA, which may comprise cellular debris and pathogen genomes. Here we investigate the phenomenon and mechanism of cellular uptake and intracellular fate of exogenous circRNAs. Human myeloid cells and B cells selectively internalize extracellular circRNAs. Macrophage uptake of circRNA is rapid, energy-dependent, and saturable. CircRNA uptake can lead to translation of encoded sequences and antigen presentation. The route of internalization influences immune activation after circRNA uptake, with distinct gene expression programs depending on the route of RNA delivery. Genome-scale CRISPR screens and chemical inhibitor studies nominate macrophage scavenger receptor MSR1, toll-like receptors, and mTOR signaling as key regulators of receptor-mediated phagocytosis of circRNAs, a dominant pathway to internalize circRNAs in parallel to macropinocytosis. These results suggest that cell-free circRNA serves as an “eat me†signal and danger-associated molecular pattern, indicating orderly pathways of recognition and disposal. eTOC Blurb: Amaya et. al. explores how cells take up extracellular circular RNAs (CircRNAs) and their impact on immune signaling. Macrophages readily internalize circRNAs, and this study identifies the specific receptors and signaling pathways governing circRNA internalization, highlighting their role as signaling molecules for immune recognition and disposal. Graphical AbstractCatalog #: Product Name: 19058 EasySep™ Human Monocyte Enrichment Kit without CD16 Depletion 19059 EasySep™ Human Monocyte Enrichment Kit Catalog #: 19058 Product Name: EasySep™ Human Monocyte Enrichment Kit without CD16 Depletion Catalog #: 19059 Product Name: EasySep™ Human Monocyte Enrichment Kit Reference(May 2024) iScience 27 6Moderate-intensity aerobic exercise training improves CD8
SummaryAerobic exercise training (AET) has emerged as a strategy to reduce cancer mortality, however, the mechanisms explaining AET on tumor development remain unclear. Tumors escape immune detection by generating immunosuppressive microenvironments and impaired T cell function, which is associated with T cell mitochondrial loss. AET improves mitochondrial content and function, thus we tested whether AET would modulate mitochondrial metabolism in tumor-infiltrating lymphocytes (TIL). Balb/c mice were subjected to a treadmill AET protocol prior to CT26 colon carcinoma cells injection and until tumor harvest. Tissue hypoxia, TIL infiltration and effector function, and mitochondrial content, morphology and function were evaluated. AET reduced tumor growth, improved survival, and decreased tumor hypoxia. An increased CD8+ TIL infiltration, IFN-γ and ATP production promoted by AET was correlated with reduced mitochondrial loss in these cells. Collectively, AET decreases tumor growth partially by increasing CD8+ TIL effector function through an improvement in their mitochondrial content and function. Graphical abstract Highlights•Exercise training reduces tumor growth and improves survival in colorectal cancer•Trained mice present tumors with less hypoxia and higher CD8+ T cells infiltration•The production of IFNγ by CD8+ TIL is increased in exercise-trained mice•CD8+ TIL from trained mice show higher mitochondrial density and function Natural sciences; Biological sciences; Biochemistry; Physiology; Immunology; Systems biology; Cancer systems biologyCatalog #: Product Name: 18953 EasySep™ Mouse CD8a Positive Selection Kit II Catalog #: 18953 Product Name: EasySep™ Mouse CD8a Positive Selection Kit II Items 1429 to 1440 of 13914 total
Shop ByFilter Results- Resource Type
-
- Product Information Sheet 2907 items
- Reference 7892 items
- Safety Data Sheet 3052 items
- Technical Manual 63 items
- Product Type
-
- 35 items
- Cell Culture Media and Supplements 27 items
- Cell Engineering and Molecular Tools 3 items
- Cell Isolation Products 5 items
- Instruments and Software 4 items
- Tissue and Cell Culture Dissociation Reagents 2 items
- Training and Education 1 item
- Area of Interest
-
- 29 items
- Angiogenic Cell Research 49 items
- Antibody Development 1 item
- Cancer 601 items
- Cell Line Development 137 items
- Cell Therapy Development 1 item
- Chimerism 5 items
- Cord Blood Banking 25 items
- Disease Modeling 4 items
- Drug Discovery and Toxicity Testing 182 items
- Endothelial Cell Biology 2 items
- Epithelial Cell Biology 158 items
- HIV 52 items
- HLA 8 items
- Hybridoma Generation 1 item
- Immunology 743 items
- Infectious Diseases 4 items
- Neuroscience 491 items
- Organoids 1 item
- Respiratory Research 1 item
- Stem Cell Biology 2493 items
- Transplantation Research 54 items
- Brand
-
- 0 20 items
- ALDECOUNT 7 items
- ALDEFLUOR 216 items
- AggreWell 55 items
- ArciTect 1 item
- BrainPhys 45 items
- CellPore 1 item
- ClonaCell 84 items
- CryoStor 65 items
- ES-Cult 77 items
- EasyPick 1 item
- EasySep 752 items
- EpiCult 12 items
- HepatiCult 1 item
- ImmunoCult 7 items
- IntestiCult 142 items
- Lymphoprep 9 items
- MammoCult 45 items
- MegaCult 34 items
- MesenCult 133 items
- MethoCult 444 items
- MyeloCult 64 items
- MyoCult 2 items
- NeuroCult 353 items
- NeuroFluor 1 item
- PancreaCult 3 items
- PneumaCult 78 items
- RSeT 7 items
- ReLeSR 1 item
- RoboSep 23 items
- RosetteSep 253 items
- STEMdiff 54 items
- STEMvision 3 items
- SepMate 29 items
- StemSpan 219 items
- TeSR 1456 items
- ThawSTAR 1 item
- mFreSR 3 items
- Cell and Tissue Source
-
- 24 items
- Cell Line
-
- 24 items
- Cell Type
-
- 27 items
- Airway Cells 41 items
- B Cells 134 items
- Brain Tumor Stem Cells 81 items
- Cancer Cells and Cell Lines 116 items
- Cardiomyocytes, PSC-Derived 8 items
- Dendritic Cells 59 items
- Dermal Cells 1 item
- Endoderm, PSC-Derived 1 item
- Endothelial Cells 1 item
- Endothelial Cells, PSC-Derived 1 item
- Epithelial Cells 49 items
- Granulocytes and Subsets 61 items
- Hematopoietic Stem and Progenitor Cells 777 items
- Hepatic Cells 2 items
- Hybridomas 75 items
- Innate Lymphoid Cells 3 items
- Intestinal Cells 13 items
- Kidney Cells 1 item
- Leukemia/Lymphoma Cells 8 items
- Leukopaks 1 item
- Mammary Cells 68 items
- Mesenchymal Stem and Progenitor Cells 132 items
- Monocytes 105 items
- Mononuclear Cells 33 items
- Myeloid Cells 99 items
- NK Cells 80 items
- Neural Cells, PSC-Derived 17 items
- Neural Stem and Progenitor Cells 381 items
- Neurons 135 items
- Plasma 3 items
- Pluripotent Stem Cells 1689 items
- Prostate Cells 7 items
- Renal Cells 2 items
- T Cells 179 items
- T Cells, CD4+ 85 items
- T Cells, CD8+ 49 items
- T Cells, Regulatory 18 items
- Species
-
- 41 items
Loading...Copyright © 2025 º£½ÇÆÆ½â°æ. All rights reserved.