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Development of a new fusion-enhanced oncolytic immunotherapy platform based on herpes simplex virus type 1.

Oncolytic viruses preferentially replicate in tumors as compared to normal tissue and promote immunogenic cell death and induction of host systemic anti-tumor immunity. HSV-1 was chosen for further development as an oncolytic immunotherapy in this study as it is highly lytic, infects human tumor cells broadly, kills mainly by necrosis and is a potent activator of both innate and adaptive immunity. HSV-1 also has a large capacity for the insertion of additional, potentially therapeutic, exogenous genes. Finally, HSV-1 has a proven safety and efficacy profile in patients with cancer, talimogene laherparepvec (T-VEC), an oncolytic HSV-1 which expresses GM-CSF, being the only oncolytic immunotherapy approach that has received FDA approval. As the clinical efficacy of oncolytic immunotherapy has been shown to be further enhanced by combination with immune checkpoint inhibitors, developing improved oncolytic platforms which can synergize with other existing immunotherapies is a high priority. In this study we sought to further optimize HSV-1 based oncolytic immunotherapy through multiple approaches to maximize: (i) the extent of tumor cell killing, augmenting the release of tumor antigens and danger-associated molecular pattern (DAMP) factors; (ii) the immunogenicity of tumor cell death; and (iii) the resulting systemic anti-tumor immune response.

1810 related Products with: Development of a new fusion-enhanced oncolytic immunotherapy platform based on herpes simplex virus type 1.

Goat Anti-Herpes Simplex Mouse Anti-Herpes Simplex Goat Anti-Herpes Simplex Goat Anti-Herpes Simplex Goat Anti-Herpes Simplex Herpes Simplex Virus 1 (H Mouse Anti-Feline Herpes Mouse Anti-Dengue Virus T Recombinant Herpes Simple Herpesvirus Type 1 (BHV 1 Human anti-parainfluenza Recombinant Herpes Simple

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Down-regulation of taurine-up-regulated gene 1 attenuates inflammation by sponging miR-9-5p via targeting NF-κB1/p50 in multiple sclerosis.

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system characterized by widespread inflammation. LncRNA taurine-up-regulated gene 1 (TUG1) has been reported to be involved in multiple biological processes and human diseases. The aim of this study was to investigate the role of lncRNA TUG1 in MS and the underlying mechanism.

1987 related Products with: Down-regulation of taurine-up-regulated gene 1 attenuates inflammation by sponging miR-9-5p via targeting NF-κB1/p50 in multiple sclerosis.

Inflammation (Mouse) Quan Inflammation (Human) Quan RubyGlowTM Luminescent Ce Inflammation (Human) Quan DNA (cytosine 5) methyltr Inflammation (Rat) Quanti Inflammation (Human) Quan Cathepsin K Blocking Pept alkaline phosphatase (int 2ml Clear vial, 8-425 scr Rat Insulin-like Growth F Mouse Inflammation Array

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Supplementary granulocyte macrophage colony-stimulating factor to chemotherapy and programmed death-ligand 1 blockade decreases local recurrence after surgery in bladder cancer.

Despite advances and refinements in surgery and perioperative chemotherapy, there are still unmet medical needs with respect to radical cystectomy for muscle-invasive bladder cancer (MIBC). We investigated the potential benefit of supplementary granulocyte macrophage colony-stimulating factor (GM-CSF) to chemoimmunotherapy with programmed cell death protein-1 (PD-1)/programmed death-ligand 1 (PD-L1) axis blockade and standard neoadjuvant chemotherapy in bladder cancer. We inoculated 2 × 10 MBT2 cells s.c. in C3H mice to create a syngeneic animal model of local recurrence (LR). When the tumor diameter reached 12 mm, the mice were allocated randomly as follows: (i) non-treated control (vehicle only); (ii) anti-mPD-L1 monotherapy; (iii) mGM-CSF monotherapy; (iv) anti-mPD-L1 plus mGM-CSF; (v) gemcitabine and cisplatin (GC); (vi) GC plus anti-mPD-L1; (vii) GC plus mGM-CSF; and (viii) GC plus anti-mPD-L1 plus mGM-CSF. After completing 2-week neoadjuvant therapy, tumors were resected for resection margin evaluation and immunohistochemical staining and blood was collected for flow cytometry and ELISA. Operative wounds were sutured, and the operative site was monitored to detect LR. Addition of anti-mPD-L1 and mGM-CSF to neoadjuvant GC chemotherapy enhanced the antitumor effect and reduced positive resection margins (50% vs 12.5%). Combination of GC, anti-mPD-L1, and mGM-CSF resulted in longer LR-free survival and cancer-specific survival compared to those in other groups. These effects involved an immunotherapy-related decrease in oncological properties such as tumor invasion capacity and epithelial-mesenchymal transition. mGM-CSF significantly decreased the accumulation of myeloid-derived suppressor cells in both the blood and tumor microenvironment and blood interleukin-6 levels. Supplementary GM-CSF to neoadjuvant GC plus PD-L1 blockade could decrease LR after radical surgery by immune modulation in the blood and tumor microenvironment.

2765 related Products with: Supplementary granulocyte macrophage colony-stimulating factor to chemotherapy and programmed death-ligand 1 blockade decreases local recurrence after surgery in bladder cancer.

Rat Granulocyte Macrophag Macrophage Colony Stimula MACROPHAGE COLONY STIMULA Human Granulocyte Macroph MACROPHAGE COLONY STIMULA CELLKINES MACROPHAGE COLO CELLKINES MACROPHAGE COLO Macrophage Colony Stimula Mouse Macrophage Colony S Mouse Granulocyte Colony Macrophage Colony Stimula Macrophage Colony Stimula

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A sensitive and rapid chemiluminescence immunoassay for point-of-care testing (POCT) of copeptin in serum based on high-affinity monoclonal antibodies via cytokine-assisted immunization.

Antibodies are key reagents in the development of immunoassay. We attempted to develop high-performance CPP immunoassays using high-affinity monoclonal antibodies prepared via cytokine-assisted immunization. We used fetal liver tyrosine kinase 3 ligand (Flt3L), CC subtype chemokine ligand 20 (CCL20), and granulocyte-macrophage colony-stimulating factor (GM-CSF) to assist traditional subcutaneous immunization of preparing high-affinity monoclonal antibodies, and further to develop high-performance immunoassay methods for CPP. This novel immune strategy significantly enhanced immune response against CPP. Six anti-CPP monoclonal antibodies (mAbs) with high affinity were successfully screened and selected for application in a fully automated magnetic chemiluminescence immunoassay (CLIA). This robust and rapid assay can efficiently detect CPP in the range of 1.2-1250 pmol L with a detection limit of 6.25 pmol L. Significantly, the whole incubation process can be completed in 30 min as compared to about 4.5 hr for the control ELISA kit. Furthermore, this assay exhibited high sensitivity and specificity, low intra-assay and inter-assay coefficients of variation (CVs < 15%). The developed assay was applied in the detection of CPP in 115 random serum samples and results showed a high correlation with data obtained using a commercially available ELISA kit (correlation coefficient, 0.9737). Our assay could be applied in the point-of-care testing of CPP in the serum samples, and also the method developed in this study could be adopted to explore the detection and diagnosis of other biomarkers for various diseases.

2858 related Products with: A sensitive and rapid chemiluminescence immunoassay for point-of-care testing (POCT) of copeptin in serum based on high-affinity monoclonal antibodies via cytokine-assisted immunization.

Cytokine (Human) Antibody Monoclonal Antibodies to Cytokine (Mouse) Antibody Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Cytokine (Human) Antibody Cytokine (Rat) Antibody A Cytokine (Human) Antibody Rat monoclonal anti mouse Cytokine (Human) Antibody Human Serum Albumin antib

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Development of anti-Müllerian hormone immunoassay based on biolayer interferometry technology.

Anti-Müllerian hormone (AMH) is a biomarker for the assessment of female fertility. The accurate measurement of the concentration of AMH is relevant for the success of assisted reproductive therapies and diagnosis of clinical cases. In this study, we show that cytokines such as fetal liver tyrosine kinase 3 ligand (Flt3L), CC subtype chemokine ligand 20 (CCL20), granulocyte-macrophage colony-stimulating factor (GM-CSF), and β-microglobulin (βM) significantly enhance the immune response against AMH. Two anti-AMH monoclonal antibodies (mAbs) with high affinity were selected by biolayer interferometry (BLI) technology for application in a fully automated magnetic chemiluminescence immunoassay (CLIA). This robust and rapid assay can efficiently detect AMH in the range of 0.125~20 ng mL with a detection limit of 0.099 ng mL. This immunoassay showed high specificity with no cross-reaction with structurally related proteins and some of the other members of the TGF-β super family, such as inhibin A, activin A, follicle-stimulating hormone, and luteinizing hormone. The average recovery rates of three different batches were 100.19%, 102.72%, and 103.59%, respectively, with coefficients of variation of less than 12%. The developed assay was applied in the detection of AMH in 69 serum samples from randomly selected patients. Our data showed a high correlation with those obtained using commercially available ELISA kits (correlation coefficient, 0.9831). Hence, we suggest that this immunoassay could find application in the development of POCT for the diagnosis of AMH in clinical samples. Graphical abstract.

2752 related Products with: Development of anti-Müllerian hormone immunoassay based on biolayer interferometry technology.

Bovine Mullerian Inhibiti Mouse Anti hPTH PTH rP Ta Mouse Anti-Growth Hormone Mouse Anti-Human Thyroid Mouse Anti-Human Growth H Mouse Anti-Human Thyroid Mouse Anti-HPV 18 Oncopro Rat monoclonal anti mouse Custom Immunoassay Develo Rabbit Anti-Follicle Stim Mouse Anti-Follicle Stimu Mouse anti human Growth H

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Pro-inflammatory responses induced by and in various human macrophage models.

Exposure to mold-contaminated indoor air has been associated with various respiratory diseases, and there is a need for experimental data to confirm these associations. The pro-inflammatory properties of well-characterized aerosolized spores and hyphal fragments from and were examined and compared using various human macrophage cell models including phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 macrophages (THP-1 Ma), primary peripheral blood monocyte-derived macrophages (MDM), and primary airway macrophages (AM) from induced sputum. X-ray treated samples of the two mold species induced different responses with displaying the most potent induction of pro-inflammatory responses. While hyphal fragments from were more potent than spores, similar responses were produced by the two growth stages of . THP-1 Ma was the most sensitive model releasing a broad range of cytokines/chemokines. MDM exhibited a similar cytokine/chemokine profile as THP-1 Ma, except for a low-quantity release of interleukin-1β (IL-1β). In contrast, AM appeared to be nonresponsive and yielded a different pattern of pro-inflammatory markers. Toll-like receptor (TLR)4, but also to a certain degree TLR2, was involved in several responses induced by spores and aerosolized hyphal fragments of in MDM. Taken together, MDM seems to be the most promising experimental macrophage model. : AF: ; AV: ; AM: Airway Macrophage; CBA: Cytometric Bead Array; CD: Cluster of Differentiation; DTT: dithiothreitol; ELISA: Enzyme Linked Immunosorbent Assay; FBS: fetal bovine serum; GM-CSF: Granulocyte macrophage colony-stimulating factor; IL-1β: Interleukin-1beta; MDM: Monocyte-Derived Macrophages; NF-κB: Nuclear Factor kappa light chain enhancer of activated B cells; NLR: NOD-like Receptor; PAMP: Pathogen Associated Molecular Pattern; PMA: Phorbol 12-myristate 13-acetate; PRR: Pattern Recognition Receptor; THP-1: Human leukemia monocyte cell line; TLR: Toll-like Receptor; TNF-α: Tumor Necrosis Factor- alpha.

2231 related Products with: Pro-inflammatory responses induced by and in various human macrophage models.

Human Macrophage Inflamma Human Macrophage Inflamma Human Gro g Macrophage In Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human, Allograft Inflamma Mouse Macrophage Inflamma Rabbit Anti-Human Apoptos Anti AGO2 Human, Monoclon Macrophage Colony Stimula TGF beta induced factor 2

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Evaluation of pro‑ and anti‑tumor effects induced by three colony‑stimulating factors, G‑CSF, GM‑CSF and M‑CSF, in bladder cancer cells: Is G‑CSF a friend of bladder cancer cells?

Cytotoxic chemotherapy is the standard treatment for patients with advanced bladder cancer. However, this treatment can cause transient and prolonged neutropenia, which can result in fatal infection. Three recombinant human colony‑stimulating factors (CSFs), granulocyte CSF (G‑CSF), granulocyte‑macrophage CSF (GM‑CSF), and macrophage CSF (M‑CSF), are currently available to reduce the duration and degree of neutropenia. The present study investigated the pro‑ and anti‑tumor effects of these three CSFs and the changes in molecular profiles. Xenograft tumors in athymic mice were generated by subcutaneously inoculating the human bladder cancer cell lines MGH‑U3 and UM‑UC‑3. A total of 2 weeks after cell inoculation, mice were randomly divided into four groups (control, G‑CSF, GM‑CSF and M‑CSF) and treated thrice a week for 2 weeks. Tumor growth during monitoring and tumor weight at the time of euthanization were significantly higher in mice treated with G‑CSF and lower in mice treated with GM‑CSF compared with the control mice. Tumors were examined by immunostaining with antibodies against proteins associated tumor proliferation (Ki‑67), angiogenesis [CD31 and vascular endothelial growth factor (VEGF)], anti‑immunity (CD204) and epithelial‑mesenchymal transition (EMT; E‑cadherin). Immunohistochemical staining revealed that tumor proliferation, angiogenesis, recruitment of M2 macrophages and EMT were promoted by G‑CSF, whereas lymphangiogenesis and recruitment of M2 macrophages were inhibited by GM‑CSF. Treatment‑associated changes in serum pro‑ and anti‑tumoral cytokines and chemokines were evaluated by enzyme‑linked immunosorbent assay (ELISA)‑based arrays. In the ELISA for serum, the levels of cytokines associated with angiogenesis (interleukin‑6 and VEGF), and EMT (transforming growth factor‑β1 and ‑β2) were elevated in mice treated with G‑CSF. Treatment with GM‑CSF and M‑CSF also affected the level of these cytokines characteristically. The current results indicate that administration of exogenous G‑CSF to patients with bladder cancer promotes tumor growth through promotion of cell proliferation, angiogenesis, recruitment of M2 macrophages and enhancement of EMT through the modulation of the tumor microenvironment.

1665 related Products with: Evaluation of pro‑ and anti‑tumor effects induced by three colony‑stimulating factors, G‑CSF, GM‑CSF and M‑CSF, in bladder cancer cells: Is G‑CSF a friend of bladder cancer cells?

Bladder cancer test tissu Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer test tissu Bladder cancer tissue arr Bladder cancer test tissu Bladder cancer and normal Mid advanced stage bladde Mid advanced stage bladde

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Sym021, a promising anti-PD1 clinical candidate antibody derived from a new chicken antibody discovery platform.

Discovery of therapeutic antibodies is a field of intense development, where immunization of rodents remains a major source of antibody candidates. However, high orthologue protein sequence homology between human and rodent species disfavors generation of antibodies against functionally conserved binding epitopes. Chickens are phylogenetically distant from mammals. Since chickens generate antibodies from a restricted set of germline genes, the possibility of adapting the Symplex antibody discovery platform to chicken immunoglobulin genes and combining it with high-throughput humanization of antibody frameworks by "mass complementarity-determining region grafting" was explored. Hence, wild type chickens were immunized with an immune checkpoint inhibitor programmed cell death 1 (PD1) antigen, and a repertoire of 144 antibodies was generated. The PD1 antibody repertoire was successfully humanized, and we found that most humanized antibodies retained affinity largely similar to that of the parental chicken antibodies. The lead antibody Sym021 blocked PD-L1 and PD-L2 ligand binding, resulting in elevated T-cell cytokine production in vitro. Detailed epitope mapping showed that the epitope recognized by Sym021 was unique compared to the clinically approved PD1 antibodies pembrolizumab and nivolumab. Moreover, Sym021 bound human PD1 with a stronger affinity (30 pM) compared to nivolumab and pembrolizumab, while also cross-reacting with cynomolgus and mouse PD1. This enabled direct testing of Sym021 in the syngeneic mouse in vivo cancer models and evaluation of preclinical toxicology in cynomolgus monkeys. Preclinical in vivo evaluation in various murine and human tumor models demonstrated a pronounced anti-tumor effect of Sym021, supporting its current evaluation in a Phase 1 clinical trial. Abbreviations: ADCC, antibody-dependent cellular cytotoxicity; CD, cluster of differentiation; CDC, complement-dependent cytotoxicity; CDR, complementarity determining region; DC, dendritic cell; ELISA, enzyme-linked immunosorbent assay; FACS, fluorescence activated cell sorting; FR, framework region; GM-CSF, granulocyte-macrophage colony-stimulating factor; HRP, horseradish peroxidase; IgG, immunoglobulin G; IL, interleukin; IFN, interferon; mAb, monoclonal antibody; MLR, mixed lymphocyte reaction; NK, natural killer; PBMC, peripheral blood mono-nuclear cell; PD1, programmed cell death 1; PDL1, programmed cell death ligand 1; RT-PCR, reverse transcription polymerase chain reaction; SEB, Staphylococcus Enterotoxin B; SPR, surface Plasmon Resonance; VL, variable part of light chain; VH, variable part of heavy chain.

2619 related Products with: Sym021, a promising anti-PD1 clinical candidate antibody derived from a new chicken antibody discovery platform.

Rabbit Anti-FMRP Polyclon Rabbit Anti-phospho-AQP2( Rabbit Anti-intestinal FA Rabbit Anti-GCK Glucokina Rabbit Anti-Cullin 5 CUL5 Rabbit Anti-AIFM3 Polyclo Rabbit Anti-PAICS Polyclo Rabbit Anti-NSE ENO2 Poly Rabbit Anti-CSNK1D Casein Rabbit Anti-HIPK2 Polyclo Mouse Anti-Chicken Bu-1a- Mouse Anti-Chicken Bu-1b-

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Incorporation of CD40 ligand or granulocyte-macrophage colony stimulating factor into Hantaan virus (HTNV) virus-like particles significantly enhances the long-term immunity potency against HTNV infection.

Hantavirus infections cause severe haemorrhagic fever with renal syndrome (HFRS) in humans and are associated with high fatality rates. In 2017, numerous outbreaks were reported in China and Germany. This represents a significant public-healthcare issue with no effective HFRS vaccines that offer a long-term immune response. In this study, we investigated the long-term humoral and cellular immune responses and protective immunity of Hantaan virus (HTNV) granulocyte-macrophage colony stimulating factor (GM-CSF) and CD40 ligand (CD40L) virus-like particles (VLPs) in mice.

2622 related Products with: Incorporation of CD40 ligand or granulocyte-macrophage colony stimulating factor into Hantaan virus (HTNV) virus-like particles significantly enhances the long-term immunity potency against HTNV infection.

Human Granulocyte Macroph Rat Granulocyte Macrophag Macrophage Colony Stimula MACROPHAGE COLONY STIMULA Human Granulocyte Colony Macrophage Colony Stimula Macrophage Colony Stimula G CSF | granulocyte colon MACROPHAGE COLONY STIMULA Human Macrophage Colony S Macrophage Colony Stimula Mouse Granulocyte Macroph

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Macrophage Polarization is Deregulated in Haemophilia.

Macrophages make important contributions to inflammation and wound healing. We show here that macrophage polarization is deregulated in haemophilia in response to macrophage colony-stimulating factor (M-CSF) and partially in response to granulocyte-macrophage colony-stimulating factor (GM-CSF). As a result, haemophilia macrophages exhibit a specific impairment of M-CSF-mediated functions involved in wound healing such as clot invasion and phagocytosis. Haemophilia monocytes express reduced amounts of the receptors for M-CSF and GM-CSF, which correlates with a failure to express tumour necrosis factor α (TNFα) and CD163 in M-CSF-treated haemophilia macrophages and reduced expression of TNFα and CD206 after treatment with GM-CSF. Protein expression in response to M-CSF was regained with respect to CD163 and CD206 after embedding haemophilia monocytes in clotted plasma suggesting that a functioning coagulation system has positive effects on macrophage M2 polarization. Mimicking the functional deficits of haemophilia macrophages in normal macrophages was possible by adding leptin, which we found to be elevated in the blood of haemophilia patients, to a monocyte cell line. The increase of leptin occurred in conjunction with C-reactive protein in a body mass index-controlled cohort suggesting that haemophilia patients harbour chronic low-grade inflammation. Together, our data indicate that impaired clotting in haemophilia patients leads to increased inflammation and a deregulation in macrophage differentiation, which may explain the commonly observed deficits in wound healing and tissue regeneration.

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