Academic literature on the topic 'Sequential common gamma chain cytokines'

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Journal articles on the topic "Sequential common gamma chain cytokines"

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Noah, T. L., and S. Becker. "Respiratory syncytial virus-induced cytokine production by a human bronchial epithelial cell line." American Journal of Physiology-Lung Cellular and Molecular Physiology 265, no. 5 (November 1, 1993): L472—L478. http://dx.doi.org/10.1152/ajplung.1993.265.5.l472.

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Respiratory syncytial virus (RSV) is the most common cause of lower respiratory infection in infants and young children, but the pathogenesis of RSV-induced inflammation is not well defined. We hypothesized that in vitro infection of a human bronchial epithelial cell line (BEAS) would induce production of proinflammatory cytokines. BEAS cells were infected with RSV, and cells and supernatants were assayed for cytokine mRNA and protein changes at several time points after infection. Cytokine mRNA in BEAS cells was measured by polymerase chain reaction of reverse-transcribed RNA from whole cell lysates; cytokine levels in supernatants were measured by bioassay or immunoassay. Our results indicated that interleukin-5ay or immunoassay. Our results indicated that interleukin-8 (IL-8) was induced at 4 h after infection (during the eclipse phase of RSV infection) with accumulation of IL-8 in supernatants by 24 h after infection. Increased levels of IL-6 and granulocyte macrophage colony-stimulating factor in supernatants were only detected by 96 h after infection, during the RSV replicative phase. Interferon-alpha and -gamma transcripts were not detectable at any time point. We conclude that the effects of RSV on airway inflammation may be at least partly mediated by sequential production of proinflammatory cytokines in infected airway epithelium.
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Zambidis, Elias T., Bruno Peault, Fred Bunz, and Curt I. Civin. "Embryonic Erythropoiesis and Definitive Hematopoiesis from Human Embryonic Stem Cells Is Regulated by Cytokines Controlling HSC Growth." Blood 104, no. 11 (November 16, 2004): 2777. http://dx.doi.org/10.1182/blood.v104.11.2777.2777.

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Abstract Human embryonic stem cells (hESC) provide an invaluable tool for studying the earliest events in human hematopoietic stem cell (HSC) development. We describe novel protocols for the efficient, step-wise differentiation of hESC to embryonic (primitive) erythroid cells and definitive erythro-myeloid cells from embryoid bodies (EB) in semi-solid and liquid cultures. EB cells were re-cultured in semisolid cultures with a cocktail of hematopoietic growth factors at different time points using a modified EB differentiation protocol, and hematopoietic differentiation was analyzed in vitro. The initiation of hematopoiesis, in this model, begins during the first week of EB differentiation. with the formation of primitive macrophages and CD31+/VE-cadherin+ hemato-endothelial clusters that “bud off” primitive embryonic hemoglobin-expressing erythroblasts and multi-potential blast colonies. These clusters ultimately form organized yolk-sac-like structures which produce a loosely adherent primitive hematopoietic cells. After 7–9 days of EB differentiation (prior to CD45 expression), primitive nucleated erythroblast colonies arise and are characterized by a “brilliant red” hemoglobinization under phase microscopy, positivity for embryonic/fetal hemoglobins by Kleihauer-Betke, qRT-PCR assays for epsilon/zeta/gamma chain expression, and a CD71+/glycophorin A+ phenotype. Simultaneously, discrete blast colonies are also shown to develop into mixed multipotential colonies containing secondary erythro-myeloid blast cells, primitive erythroblasts, and macrophages; suggesting a common progenitor for the discrete embryonic phenotypes observed at this stage. Following this first wave of primitive hematopoiesis, definitive CD45+-expressing colony-forming cells (CFC) can be generated from EB cells differentiated for 10–15 days with the sequential appearance of BFU-E, CFU-E, GM-CFC, and multi-lineage CFC. A kinetic expression analysis using qRT-PCR methods, revealed that the first wave of embryonic hematopoiesis at 6–9 days of EB development directly coincides with expression of SCL/TAL1, AML1, GATA1, and GATA2, while the onset of definitive hematopoiesis at 9–15 days directly correlates with increased EB expression of CD34, CD31, CD41, c-myb, and cdx4. In this model, primitive hematopoiesis in EB cells proceeds in the absence of exogenously added growth factors. However, supplementing EB differentiation cultures with FLT3-ligand, KIT-ligand, and THROMBOPOIETIN (FTK), dramatically enhances the number of primitive erythroblast, and multi-lineage blast CFC, as well as the definitive BFU-E, CFU-E, and multi-potent mixed CFC. The kinetics of colony formation for both primitive and definitive CFC is unaffected by FTK supplementation. Moreover, blast cell colonies from EB cells differentiated in the presence of FTK were more potent than those generated without FTK. These blast colonies differentiate into mixed, multi-lineage CD45+/CD13+/CD41+/CD71+/glycophorin A+-expressing colonies that contain both primitive nucleated embryonic hemoglobin-expressing erythroblasts, and definitive mature beta-globin-expressing erythroid cells, neutrophils, monocytes/macrophages, and megakaryocytic precursors. This hESC model reveals the putative existence of a common human progenitor for both embryonic-type and definitive hematopoietic cells, and that cytokines known to expand/self-renew definitive HSC may potentially regulate this differentiation process.
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Shourian, Mitra, Jean-Christophe Beltra, Benoîte Bourdin, and Hélène Decaluwe. "Common gamma chain cytokines and CD8 T cells in cancer." Seminars in Immunology 42 (April 2019): 101307. http://dx.doi.org/10.1016/j.smim.2019.101307.

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Pulliam, Stephanie R., Roman V. Uzhachenko, Samuel E. Adunyah, and Anil Shanker. "Common gamma chain cytokines in combinatorial immune strategies against cancer." Immunology Letters 169 (January 2016): 61–72. http://dx.doi.org/10.1016/j.imlet.2015.11.007.

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Farhat, Ali M., Adam C. Weiner, Cori Posner, Zoe S. Kim, Brian Orcutt-Jahns, Scott M. Carlson, and Aaron S. Meyer. "Modeling cell-specific dynamics and regulation of the common gamma chain cytokines." Cell Reports 35, no. 4 (April 2021): 109044. http://dx.doi.org/10.1016/j.celrep.2021.109044.

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Querfeld, Christiane, Basem M. William, Lubomir Sokol, Oleg Akilov, Brian Poligone, Jasmine Zain, Yutaka Tagaya, and Nazli Azimi. "Co-Inhibition of IL-2, IL-9 and IL-15 By the Novel Immunomodulator, Bnz-1, Provides Clinical Efficacy in Patients with Refractory Cutaneous T Cell Lymphoma in a Phase 1/2 Clinical Trial." Blood 136, Supplement 1 (November 5, 2020): 37. http://dx.doi.org/10.1182/blood-2020-143135.

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Background: Cutaneous T cell lymphoma is incurable with current standard therapies and there is an urgent need for more effective therapies. BNZ-1 is a pegylated peptide antagonist that binds to the common gamma chain signaling receptor for cytokines IL-2, IL-9 and IL-15. We hypothesized that inhibition of these 3 cytokines could generate a therapeutic benefit to CTCL patients through a multipronged mechanism: 1) IL-2 and IL-15 inhibition blocks cytokine-driven propagation/survival of tumor cells 2) IL-2 and IL-9 inhibition lowers the activity of regulatory T-cells that may impede the anti-lymphoma immune response 3) IL-15 inhibition may provide an additional anti-inflammatory effect Methods: A multicenter, open-label Phase 1/2 study was completed to characterize the safety and efficacy of BNZ-1 (NCT03239392). Refractory patients, who have failed FDA-approved or investigational treatments appropriate for the stage of their disease, with a diagnosis of mycosis fungoides (MF) of any stage or Sézary syndrome (SS) were eligible for this trial. In part I of the study, Pts were enrolled in sequential dose cohorts of 0.5 mg/kg, 1mg/kg, 2 mg/kg, and 4 mg/kg to receive weekly intravenous dose of BNZ-1 to characterize safety, pharmacokinetics, pharmacodynamics, and evidence of antitumor activity. Thereafter, patients were enrolled on an extension phase for 3 months of weekly dosing of BNZ-1. Patients who achieved a response were eligible for a long-term extension arm. Blood samples were collected to assess the impact of BNZ-1 on PD biomarkers including Treg numbers and activation markers of cytotoxic T lymphocytes using FACS analysis. Results: In the dose ranging part of the study, 15 patients (stages IB and IVB) were enrolled across the 4 dose cohorts. All patients completed the first 4 weeks for safety of the study and 9 enrolled in the 3-month extension period and 3 continued in the long term extension (LTE) period for over a year. BNZ-1 showed activity in all doses as it was determined by early signs of clinical efficacy and PD biomarkers. Subsequently, we selected the 2 mg/kg based on PK/PD relationship and clinical efficacy and expanded to a total of 19 patients. Clinical efficacy was measured by mSWAT and Global Response Score (GRS) as defined previously (Olsen E. et al. 2011). Based on the best response, one patient (5%) achieved a complete response, eleven (58%) patients achieved a partial response (50% reduction over baseline) by the end of the study. 7 patients (37%) showed stable disease during the study period. No disease recurrence was observed during the study period. For those patients who responded to the therapy in the dose ranging part of the study, the mean duration of response was calculated to be 9.2 months. Overall, BNZ-1 was well tolerated and showed no serious treatment-related adverse events in this patient population. Furthermore, PD analysis revealed that BNZ-1 discernibly suppressed the inflammatory nature of CTLs in majority of patients that respond to BNZ-1 treatment as measured by reduction in their mSWAT scores Conclusion: BNZ-1, an IL-2, IL-9, and IL-15 inhibitor, may provide a novel treatment option for CTCL patients who relapsed or were refractory with conventional therapies with a favorable toxicity profile. The multifaceted approach of BNZ-1 leads to direct inhibition of malignant cells, activation of tumor immunity, and suppression of inflammation. Since BNZ-1 showed safety and efficacy in challenging rCTCL patient population, its further development in a phase 3 trial is planned. Disclosures Querfeld: Celgene: Research Funding; MiRagen: Consultancy; Trillium: Consultancy; Helsinn: Consultancy; Stemline: Consultancy; Bioniz: Consultancy; Kyowa Kirin: Consultancy. William:Kyowa Kirin: Consultancy, Honoraria; Dova: Research Funding; Merck: Research Funding; Celgene: Consultancy, Honoraria; Guidepoint Global: Consultancy; Incyte: Research Funding; Seattle Genetics: Research Funding. Sokol:Kymera Therapeutics: Membership on an entity's Board of Directors or advisory committees; Kyowa/Kirin Inc.: Membership on an entity's Board of Directors or advisory committees; EUSA Pharma: Consultancy, Honoraria, Speakers Bureau. Akilov:Trillium: Consultancy; Bioniz: Consultancy. Zain:Seattle Genetics: Research Funding; Mundi Pharma: Research Funding; Kyowa Kirin: Research Funding. Tagaya:Bioniz: Consultancy. Azimi:Bioniz: Current Employment.
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Scanzello, C. R., E. Umoh, T. Miles, H. G. Potter, R. Marx, S. Rodeo, S. R. Goldring, and M. K. Crow. "441 COMMON GAMMA-CHAIN CYTOKINES IN PATIENTS WITH EARLY AND END-STAGE OSTEOARTHRITIS." Osteoarthritis and Cartilage 16 (September 2008): S191—S192. http://dx.doi.org/10.1016/s1063-4584(08)60482-3.

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Pahwa, Savita. "Role of common gamma chain utilizing cytokines for immune reconstitution in HIV infection." Immunologic Research 38, no. 1-3 (June 21, 2007): 373–86. http://dx.doi.org/10.1007/s12026-007-0036-9.

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Toe, Jesse G., Marc Pellegrini, and Tak Wah Mak. "Promoting immunity during chronic infection—The therapeutic potential of common gamma-chain cytokines." Molecular Immunology 56, no. 1-2 (November 2013): 38–47. http://dx.doi.org/10.1016/j.molimm.2013.04.008.

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Meazza, Raffaella, Bruno Azzarone, Anna Maria Orengo, and Silvano Ferrini. "Role of Common-Gamma Chain Cytokines in NK Cell Development and Function: Perspectives for Immunotherapy." Journal of Biomedicine and Biotechnology 2011 (2011): 1–16. http://dx.doi.org/10.1155/2011/861920.

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NK cells are components of the innate immunity system and play an important role as a first-line defense mechanism against viral infections and in tumor immune surveillance. Their development and their functional activities are controlled by several factors among which cytokines sharing the usage of the common cytokine-receptor gamma chain play a pivotal role. In particular, IL-2, IL-7, IL-15, and IL-21 are the members of this family predominantly involved in NK cell biology. In this paper, we will address their role in NK cell ontogeny, regulation of functional activities, development of specialized cell subsets, and acquisition of memory-like functions. Finally, the potential application of these cytokines as recombinant molecules to NK cell-based immunotherapy approaches will be discussed.
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Dissertations / Theses on the topic "Sequential common gamma chain cytokines"

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Basu, Debasmita. "EX VIVO EXPANSION OF TUMOR-SPECIFIC T CELLS WITH SEQUENTIAL COMMON GAMMA CHAIN CYTOKINES RENDER THEM REFRACTORY TO MDSC UPON ADOPTIVE IMMUNOTHERAPY." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2198.

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Myeloid derived suppressor cells (MDSCs) are heterogeneous population of immature cells at various stages of differentiation, characterized by the presence of CD11b and Gr1 in mice. They are major contributors of the tumor-induced immune suppression against the tumors. So far, various strategies have been introduced to overcome the endogenous MDSCs. Most of these approaches rely on the elimination of MDSCs and it is not clear whether tumor-reactive T cells may be differentiated towards phenotypes that are refractory to MDSCc. Our laboratory has previously shown that high affinity T cells derived from tumor-sensitized wild-type FVB mice and expanded ex vivo with the alternating common gamma chain cytokine formulation (initiation of culture with IL-7 + IL-15 followed by one day pulse with IL-2 and continuation of culture with IL-7 + IL-15) can successfully induce tumor regression in FVBN202 transgenic mouse model of breast carcinoma upon adoptive immunotherapy (AIT), only when combined with the depletion of endogenous MDSCs. In this study we have introduced a novel formulation of the sequential common gamma chain cytokines (initiation of culture with IL-7 + IL-15 followed by the expansion with IL-2 until 6 days) for the ex vivo expansion of the autologous and tumor-sensitized low affinity T cells derived from FVBN202 mice and further used for AIT. This novel formulation induced differentiation of tumor-reactive CD8+ T cells mainly towards effector and effector/memory phenotypes that were refractory to MDSCs in vitro and in vivo. AIT by using these T cells induced rejection of primary neu positive tumors and generated long-term memory responses against the recall tumor challenge. Importantly, these T cells also resulted in the inhibition of neu antigen negative relapsed tumor cells. Our findings in the present study provide a platform for AIT of breast cancer patients. .
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Hall, Charles. "Ex vivo reprogramming of tumor-reactive immune cells from FVBN202 mice bearing lung metastatic mammary carcinoma: an immunotherapeutic opportunity revealed against recurrence." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3176.

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Metastatic breast cancer treatment has seen few advances in recent years, yet treatment resistance continues to rise, causing disease recurrence. A pilot study was performed to determine the efficacy of ex vivo expansion and reprogramming of tumor-reactive immune cells from experimental metastatic tumor-sensitized mice. Also, phenotypic changes in tumors due to metastasis or tumor microenvironment influences were characterized. Metastatic neu+ mouse mammary carcinoma (mMMC) and its distant relapsing neu-antigen-negative variant (mANV) were investigated in FVBN202 mice. Tumor-reactive central memory CD8+ T cells and activated NK/NKT cells were successfully reprogrammed and expanded during 6-day expansion from mMMC- and/or mANV-sensitized mice, resulting in tumor-specific cytotoxicity. mMMC exhibited a flexible neu-expression pattern and acquired stem-like, tumorigenic phenotype following metastasis while mANV remained stable except decreased tumorigenicity. Myeloid-derived suppressor cell (MDSC) levels were not increased. Adoptive cellular therapy (ACT) with reprogrammed tumor-reactive immune cells may prove effective prophylaxis against metastatic or recurrent breast cancer.
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Book chapters on the topic "Sequential common gamma chain cytokines"

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Girard, D. "Phenotypic and Functional Change of Neutrophils Activated by Cytokines Utilizing the Common Cytokine Receptor Gamma Chain." In Chemical Immunology and Allergy, 64–80. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071565.

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Blom, B., H. Spits, and P. Krimpenfort. "The Role of the Common Gamma Chain of the IL-2, IL-4, IL-7 and IL-15 Receptors in Development of Lymphocytes. Constitutive Expression of Bcl-2 does not Rescue the Developmental Defects in Gamma Common-Deficient Mice." In Cytokines and Growth Factors in Blood Transfusion, 3–11. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4613-1137-9_1.

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Conference papers on the topic "Sequential common gamma chain cytokines"

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Payne, Kyle K., Maciej Kmieciak, Debasmita Basu, Viswanathan Ramakrishnan, Harry D. Bear, and Masoud H. Manjili. "Abstract 775: Sequential common gamma-chain cytokines facilitate differentiation of tumor-reactive T cells that are resistant to MDSC and can induce rejection of breast tumors." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-775.

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Mengus, Chantal, Clémentine Le Magnen, Lukas Bubendorf, Alexander Bachmann, Michael Heberer, Giulio C. Spagnoli, and Stephen Wyler. "Abstract 3658: The expression of genes encoding common gamma-chain cytokines is associated with tissue infiltration by CD8+ T cells displaying an “exhausted” phenotype in benign prostatic hyperplasia and prostate cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3658.

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