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#33936816   2021/04/14 To Up

Sunitinib Combined with Th1 Cytokines Potentiates Apoptosis in Human Breast Cancer Cells and Suppresses Tumor Growth in a Murine Model of HER-2 Breast Cancer.

Although immune-based therapies have made remarkable inroads in cancer treatment, they usually must be combined with standard treatment modalities, including cytotoxic drugs, to achieve maximal clinical benefits. As immunotherapies are further advanced and refined, considerable efforts will be required to identify combination therapies that will maximize clinical responses while simultaneously decreasing the unpleasant and sometimes life-threatening side effects of standard therapy. Over the last two decades, evidence has emerged that Th1 cytokines can play a central role in protective antitumor immunity and that combinations of Th1 cytokines can induce senescence and apoptosis in cancer cells. To explore the possibility of combining targeted drugs with Th1-polarizing vaccines, we undertook a study to examine the impact of combining Th1 cytokines with the relatively broad-spectrum receptor tyrosine kinase antagonist, sunitinib. We found that when a panel of five phenotypically diverse human breast cancer cell lines was subjected to treatment with sunitinib plus recombinant Th1 cytokines IFN- and TNF-, synergistic effects were observed across a number of parameters including different aspects of apoptotic cell death. Interestingly, sunitinib was found to have a profoundly suppressive effect of T cell's capacity to secrete IFN-, indicating that in vivo use of this drug may hinder robust Th1 responses. Nonetheless, this suppression was circumvented in a mouse model of HER-2 breast disease by supplying recombinant interferon-gamma to achieve a combination therapy significantly more potent than either agent.
Nirmala Ghimirey, Chase Steele, Brian J Czerniecki, Gary K Koski, Loral E Showalter

1032 related Products with: Sunitinib Combined with Th1 Cytokines Potentiates Apoptosis in Human Breast Cancer Cells and Suppresses Tumor Growth in a Murine Model of HER-2 Breast Cancer.



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#33908208   // To Up

Roles of Type I and III Interferons in COVID-19.

Coronavirus disease 2019 (COVID-19) is an ongoing global pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Type I and III interferon (IFN) responses act as the first line of defense against viral infection and are activated by the recognition of viruses by infected cells and innate immune cells. Dysregulation of host IFN responses has been known to be associated with severe disease progression in COVID-19 patients. However, the reported results are controversial and the roles of IFN responses in COVID-19 need to be investigated further. In the absence of a highly efficacious antiviral drug, clinical studies have evaluated recombinant type I and III IFNs, as they have been successfully used for the treatment of infections caused by two other epidemic coronaviruses, SARS-CoV-1 and Middle East respiratory syndrome (MERS)-CoV. In this review, we describe the strategies by which SARS-CoV-2 evades IFN responses and the dysregulation of host IFN responses in COVID-19 patients. In addition, we discuss the therapeutic potential of type I and III IFNs in COVID-19.
Hojun Choi, Eui Cheol Shin

2416 related Products with: Roles of Type I and III Interferons in COVID-19.

1 mg50 100.00 ug96 wells (1 kit)50ul50 10 100 μg

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#33871374   2021/04/16 To Up

Co-existence of specific IgE antibodies and T cells reactive to house dust mites and human transglutaminase3/tropomysin in patients with atopic dermatitis.

Although specific IgE antibodies reactive to exogenous antigens are found in patients with atopic dermatitis (AD), some patients do not have such antibodies. Autoimmunity has been proposed as a possible mechanism in these patients.
Jing Sun, Ying Gu, Kun Li, Jian-Zhong Zhang

2275 related Products with: Co-existence of specific IgE antibodies and T cells reactive to house dust mites and human transglutaminase3/tropomysin in patients with atopic dermatitis.

0.1 mg100 4 Arrays/Slide4 Membranes/Box100 μg4 Arrays/Slide4 Membranes/Box100 μg25mg4 Membranes/Box4 Arrays/Slide

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#33867706   2020/01/30 To Up

The Effects of Self-cleavage Intein-ELK16 Tag in the Transcript Steric Hindrance of IFN.

Intervening proteins (Inteins) are identified as protein domains in a precursor protein structure. Inteins can excise itself from precursor protein and join the remaining portions which result in forming an active protein. In this study, the transcript expression level of recombinant human Interferon beta (rhIFNβ) connected to the self-cleavage Intein-ELK16 (LELELKLKLELELKLK) tag was measured by real-time PCR in HEK293T cell line. First, the sequence of RecA (Mtu recA) was obtained from the InBase database to do appropriate changes including adding the restriction sites, kozak sequence, signal peptide and ELK16 sequence by SnapGene software. The RNA secondary structure were also examined using the online RNA Fold 2.2 web server. Next, the construct was inserted into pUC19 plasmid. The sequence of rhIFNβ was also cloned into pBudCE4.1 vector. In the next step, the rhIFNβ was ligated into the construct (self-cleavage tag of ELK16) using T4 DNA ligase and the recombinant construct was transfected into HEK293T cell line. Finally, expression of the cassette was evaluated by real-time PCR. The analysis of secondary RNA structure indicates a minimum free energy of MEF - 261.10 kcal/mol. Our results indicate that IFNβ was upregulated (37.8-fold, < 0.0001) in cells which transfected by rhIFNβ-ELK16 compared to the mock and un-transfected conditions. Altogether, our results show that the presence of mini self-cleavage Intein-ELK16 tag along with the rhIFNβ had no interference in transcription of rhIFNβ in the HEK293T cell line.
Sayed Sharif Balkhi, Zohreh Hojati

1146 related Products with: The Effects of Self-cleavage Intein-ELK16 Tag in the Transcript Steric Hindrance of IFN.

12 100 U100.00 ul

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#33862556   2021/04/13 To Up

Interleukin-35 regulates peripheral T cell activity in patients with Kawasaki disease.

Interleukin-35 (IL-35) regulates immune cell function in inflammation, infection, cancer, and autoimmune diseases. However, the modulatory activity of IL-35 exerted on T cells is not fully understood in Kawasaki disease. For this purpose, the present study included 28 patients with Kawasaki disease and 16 healthy controls. The mRNA levels of IL-35 receptor subunits, including IL-12Rβ2 and gp130, were determined by conducting real-time PCR. CD4 and CD8 T cells were enriched, and stimulated with recombinant human IL-35. The influence of IL-35 on transcription factors and cytokine secretion by CD4 T cells was assessed by performing real-time PCR and ELISA. The modulatory activity of IL-35 on CD8 T cells was investigated by measuring target cell death, perforin/granzyme B secretion, and immune checkpoint molecule expression. IL-12Rβ2 and gp130 mRNA levels were comparable in CD4 and CD8 T cells between patients with Kawasaki disease and controls. Patients with Kawasaki disease showed stronger Th1, Th17, and Th22 responses, but weaker Treg response compared with controls. IL-35 stimulation suppressed Th1, Th17, and Th22 responses but enhanced Treg response. Patients with Kawasaki disease showed elevated CD8 T cell-induced cytotoxicity. IL-35 stimulation inhibited CD8 T cell-induced target cell death. The downregulation of IFN-γ expression and perforin/granzyme B secretion, and the upregulation of PD-1, CTLA-4, and LAG-3 expression following IL-35 stimulation were responsible for decreased CD8 T cell-induced cytotoxicity. IL-35 may play a pivotal immunosuppressive role in T cell function, which may be involved in the protective mechanism against inflammation in Kawasaki disease.
Min Sun, Haijian Xing

2452 related Products with: Interleukin-35 regulates peripheral T cell activity in patients with Kawasaki disease.

1 kit11 kit96 tests 0.1 mg 10

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#33859303   2021/04/15 To Up

Sarcoma IL-12 overexpression facilitates NK cell immunomodulation.

Interleukin-12 (IL-12) is an inflammatory cytokine that has demonstrated efficacy for cancer immunotherapy, but systemic administration has detrimental toxicities. Lentiviral transduction eliciting IL-12-producing human sarcoma for autologous reintroduction provides localized delivery for both innate and adaptive immune response augmentation. Sarcoma cell lines and primary human sarcoma samples were transduced with recombinant lentivirus engineering expression of human IL-12 (hu-IL-12). IL-12 expressing sarcomas were assessed in vitro and in vivo following implantation into humanized NSG and transgenic human IL-15 expressing (NSG.Tg(Hu-IL-15)) murine models. Lentiviral transduction (LV/hu-IL-12) of human osteosarcoma, Ewing sarcoma and rhabdomyosarcoma cell lines, as well as low-passage primary human sarcomas, engendered high-level expression of hu-IL-12. Hu-IL-12 demonstrated functional viability, eliciting specific NK cell-mediated interferon-γ (IFN-γ) release and cytotoxic growth restriction of spheroids in vitro. In orthotopic xenograft murine models, the LV/hu-IL-12 transduced human sarcoma produced detectable IL-12 and elicited an IFN-γ inflammatory immune response specific to mature human NK reconstitution in the NSG.Tg(Hu-IL-15) model while restricting tumor growth. We conclude that LV/hu-IL-12 transduction of sarcoma elicits a specific immune reaction and the humanized NSG.Tg(Hu-IL-15) xenograft, with mature human NK cells, can define in vivo anti-tumor effects and systemic toxicities. IL-12 immunomodulation through autologous tumor transduction and reintroduction merits exploration for sarcoma treatment.
Mary Jo Rademacher, Anahi Cruz, Mary Faber, Robyn A A Oldham, Dandan Wang, Jeffrey A Medin, Nathan J Schloemer

2194 related Products with: Sarcoma IL-12 overexpression facilitates NK cell immunomodulation.

1 G10 mg1 g100500 ml1 kit100ug Lyophilized

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#33854293   2021/03/30 To Up

Cytokine Profiling in Plasma from Patients with Brain Tumors Versus Healthy Individuals using 2 Different Multiplex Immunoassay Platforms.

We compared the performance of two 96-well multiplex immunoassay platforms in assessing plasma cytokine concentrations in patients with glioblastoma (GBM; n = 27), individuals with melanoma, breast or lung cancer metastases to the brain (n = 17), and healthy volunteers (n = 11). Assays included a bead-based fluorescence MILLIPLEX assay/Luminex (LMX) platform and 4 planar electrochemiluminescence kits from Meso Scale Discovery (MSD). The LMX kit evaluated 21 cytokines and the 3 MSD kits evaluated 20 cytokines in total, with 19 overlapping human cytokines between platforms (GM-CSF, IFNγ, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12p70, IL-13, IL-17A, IL-21, IL-23, MIP-1α, MIP-1β, MIP-3α, TNFα). The MSD platform had lower LLoQs (lower limits of quantification) than LMX for 17/19 cytokines, and higher LLoQs for IFN-γ and IL-21. The ULoQs were higher in LMX versus MSD assays for 17/19 shared analytes, but lower than MSD for IL-17A and IL-21. With LMX, all 19 shared analytes were quantifiable in each of 55 samples. Although MSD recombinant protein standard curves indicated lower LLoQs than LMX for most cytokines, MSD detected 7/19 (37%) native analytes in <75% of samples, including 0% detection for IL-21 and 8% for IL-23. The LMX platform categorized identical samples at greater concentrations than the MSD system for most analytes (MIP-1β the sole exception), sometimes by orders of magnitude. This mismatched quantification paradigm was supported by Bland-Altman analysis. LMX identified significantly elevated levels of 10 of 19 circulating cytokines in GBM: GM-CSF, IFN-γ, IL-1β, IL-5, IL-10, IL-17A, IL-21, IL-23, MIP-1α, and MIP-3α, consistent with prior findings and confirming the utility of applying appropriate multiplex immunoassay technologies toward developing a cytokine signature profile for GBM.
Diane Elizabeth Bender, Maximilian O Schaettler, Kathleen Cf Sheehan, Tanner M Johanns, Gavin P Dunn

2392 related Products with: Cytokine Profiling in Plasma from Patients with Brain Tumors Versus Healthy Individuals using 2 Different Multiplex Immunoassay Platforms.

121 mg16 Arrays/Slide16 Arrays/Slide10 ug16 Arrays/Slide16 Arrays/Slide16 Arrays/Slide200mg

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#33848910   2021/04/11 To Up

Formulation of HBsAg in Montanide ISA 51VG adjuvant: Immunogenicity study and monitoring long-lived humoral immune responses.

Montanide ISA 51VG adjuvant has been approved for human clinical application and stimulates cellular and humoral immune responses. Here, HBsAg was formulated in Montanide ISA51VG adjuvant to compare its potency with the Fendrix and HBsAg-alum vaccines. In particular, the long-term humoral response was assessed up to 220 days after the final immunization. BALB/c mice were allocated into six groups. Treatment groups were injected with HBsAg-Montanide ISA51VG, the Fendrix and commercial HBsAg-alum, respectively. Montanide ISA51 VG, Alum and PBS injected mice were considered as control groups. Mice were immunized three times with 2-week intervals on days 0, 14 and 28 by subcutaneous injection. Lymphocyte proliferation was assessed with the BrdU method. IFN-γ, IL-2 and IL-4 cytokines, specific total IgG and IgG1/IgG2a isotypes were assessed using ELISA. The HBsAg-Montanide ISA51VG vaccine resulted in a significant increase in lymphocyte proliferation versus HBsAg-alum and higher IL-2 cytokine production versus the Fendrix. Comparable IL-4 and IFN-γ cytokines responses were observed for these vaccines. Following the first immunization, IgG increased more in HBs-Montanide 51VG group versus the HBs-alum group, while after the second and third shots comparable responses were observed in comparison to the HBs-alum group. Monitoring for 220 days after the final vaccination showed the superiority of HBsAg-Montanide ISA 51VG vaccine versus HBsAg-alum and even the Fendrix vaccine in the induction of long-term antibody responses. This study suggests that HBsAg-Montanide ISA51VG as a novel vaccine formulation can trigger both cellular and long-lasting humoral immune responses more efficiently than conventional HBsAg vaccines.
Mohammad Ali Savoji, Mohammad Mehdi Adibzadeh Sereshgi, Seyed Mohammad Mahdi Ghahari, Fatemeh Asgarhalvaei, Mehdi Mahdavi

1941 related Products with: Formulation of HBsAg in Montanide ISA 51VG adjuvant: Immunogenicity study and monitoring long-lived humoral immune responses.

500 tests100 μg100 μg96 wells (1 kit)100 μg100ug Lyophilized100ug100ug

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#33847226   2021/04/13 To Up

SARS‑CoV-2 RBD219-N1C1: A yeast-expressed SARS-CoV-2 recombinant receptor-binding domain candidate vaccine stimulates virus neutralizing antibodies and T-cell immunity in mice.

There is an urgent need for an accessible and low-cost COVID-19 vaccine suitable for low- and middle-income countries. Here, we report on the development of a SARS-CoV-2 receptor-binding domain (RBD) protein, expressed at high levels in yeast (), as a suitable vaccine candidate against COVID-19. After introducing two modifications into the wild-type RBD gene to reduce yeast-derived hyperglycosylation and improve stability during protein expression, we show that the recombinant protein, RBD219-N1C1, is equivalent to the wild-type RBD recombinant protein (RBD219-WT) in an ACE-2 binding assay. Immunogenicity studies of RBD219-N1C1 and RBD219-WT proteins formulated with Alhydrogel® were conducted in mice, and, after two doses, both the RBD219-WT and RBD219-N1C1 vaccines induced high levels of binding IgG antibodies. Using a SARS-CoV-2 pseudovirus, we further showed that sera obtained after a two-dose immunization schedule of the vaccines were sufficient to elicit strong neutralizing antibody titers in the 1:1,000 to 1:10,000 range, for both antigens tested. The vaccines induced IFN-γ IL-6, and IL-10 secretion, among other cytokines. Overall, these data suggest that the RBD219-N1C1 recombinant protein, produced in yeast, is suitable for further evaluation as a human COVID-19 vaccine, in particular, in an Alhydrogel® containing formulation and possibly in combination with other immunostimulants.
Jeroen Pollet, Wen-Hsiang Chen, Leroy Versteeg, Brian Keegan, Bin Zhan, Junfei Wei, Zhuyun Liu, Jungsoon Lee, Rahki Kundu, Rakesh Adhikari, Cristina Poveda, Maria Jose Villar, Ana Carolina de Araujo Leao, Joanne Altieri Rivera, Zoha Momin, Portia M Gillespie, Jason T Kimata, Ulrich Strych, Peter J Hotez, Maria Elena Bottazzi

2561 related Products with: SARS‑CoV-2 RBD219-N1C1: A yeast-expressed SARS-CoV-2 recombinant receptor-binding domain candidate vaccine stimulates virus neutralizing antibodies and T-cell immunity in mice.

100 100.00 ug100 100ug Lyophilized100 μg100 100.00 ug200ul100 100ug Lyophilized200ul100

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