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  1 / 637 MEDLINE  
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PMID:29324880
Autor:Zhao K; Zheng WW; Dong XM; Yin RH; Gao R; Li X; Liu JF; Zhan YQ; Yu M; Chen H; Ge CH; Ning HM; Yang XM; Li CY
Endereço:State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China.
Título:EDAG promotes the expansion and survival of human CD34+ cells.
Fonte:PLoS One; 13(1):e0190794, 2018.
ISSN:1932-6203
País de publicação:United States
Idioma:eng
Resumo:EDAG is multifunctional transcriptional regulator primarily expressed in the linloc-kit+Sca-1+ hematopoietic stem cells (HSC) and CD34+ progenitor cells. Previous studies indicate that EDAG is required for maintaining hematopoietic lineage commitment balance. Here using ex vivo culture and HSC transplantation models, we report that EDAG enhances the proliferative potential of human cord blood CD34+ cells, increases survival, prevents cell apoptosis and promotes their repopulating capacity. Moreover, EDAG overexpression induces rapid entry of CD34+ cells into the cell cycle. Gene expression profile analysis indicate that EDAG knockdown leads to down-regulation of various positive cell cycle regulators including cyclin A, B, D, and E. Together these data provides novel insights into EDAG in regulation of expansion and survival of human hematopoietic stem/progenitor cells.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Antigens, CD34); 0 (Cyclins); 0 (HEMGN protein, human); 0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit); 0 (Nuclear Proteins)


  2 / 637 MEDLINE  
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PMID:29045900
Autor:Alhaj Hussen K; Vu Manh TP; Guimiot F; Nelson E; Chabaane E; Delord M; Barbier M; Berthault C; Dulphy N; Alberdi AJ; Burlen-Defranoux O; Socié G; Bories JC; Larghero J; Vanneaux V; Verhoeyen E; Wirth T; Dalod M; Gluckman JC; Cumano A; Canque B
Endereço:INSERM U1126, Université Paris-Diderot, École Pratique des Hautes Etudes/PSL Research University, Institut Universitaire d'Hématologie, Hôpital Saint-Louis, Paris, France.
Título:Molecular and Functional Characterization of Lymphoid Progenitor Subsets Reveals a Bipartite Architecture of Human Lymphopoiesis.
Fonte:Immunity; 47(4):680-696.e8, 2017 Oct 17.
ISSN:1097-4180
País de publicação:United States
Idioma:eng
Resumo:The classical model of hematopoiesis established in the mouse postulates that lymphoid cells originate from a founder population of common lymphoid progenitors. Here, using a modeling approach in humanized mice, we showed that human lymphoid development stemmed from distinct populations of CD127 and CD127 early lymphoid progenitors (ELPs). Combining molecular analyses with in vitro and in vivo functional assays, we demonstrated that CD127 and CD127 ELPs emerged independently from lympho-mono-dendritic progenitors, responded differently to Notch1 signals, underwent divergent modes of lineage restriction, and displayed both common and specific differentiation potentials. Whereas CD127 ELPs comprised precursors of T cells, marginal zone B cells, and natural killer (NK) and innate lymphoid cells (ILCs), CD127 ELPs supported production of all NK cell, ILC, and B cell populations but lacked T potential. On the basis of these results, we propose a "two-family" model of human lymphoid development that differs from the prevailing model of hematopoiesis.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-7 Receptor alpha Subunit)


  3 / 637 MEDLINE  
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PMID:28716979
Autor:Bustamante A; López-Cancio E; Pich S; Penalba A; Giralt D; García-Berrocoso T; Ferrer-Costa C; Gasull T; Hernández-Pérez M; Millan M; Rubiera M; Cardona P; Cano L; Quesada H; Terceño M; Silva Y; Castellanos M; Garces M; Reverté S; Ustrell X; Marés R; Baiges JJ; Serena J; Rubio F; Salas E; Dávalos A; Montaner J
Endereço:From the Neurovascular Research Laboratory, Vall d'Hebron Institut de Recerca (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Spain (A.B., A.P., D.G., T.G.-B., J.M.); Stroke Unit, Hospital Universitari Germans Trias i Pujol, Barcelona, Spain (E.L.-C., M.H.-P., M.M., A
Título:Blood Biomarkers for the Early Diagnosis of Stroke: The Stroke-Chip Study.
Fonte:Stroke; 48(9):2419-2425, 2017 Sep.
ISSN:1524-4628
País de publicação:United States
Idioma:eng
Resumo:BACKGROUND AND PURPOSE: Stroke diagnosis could be challenging in the acute phase. We aimed to develop a blood-based diagnostic tool to differentiate between real strokes and stroke mimics and between ischemic and hemorrhagic strokes in the hyperacute phase. METHODS: The Stroke-Chip was a prospective, observational, multicenter study, conducted at 6 Stroke Centers in Catalonia. Consecutive patients with suspected stroke were enrolled within the first 6 hours after symptom onset, and blood samples were drawn immediately after admission. A 21-biomarker panel selected among previous results and from the literature was measured by immunoassays. Outcomes were differentiation between real strokes and stroke mimics and between ischemic and hemorrhagic strokes. Predictive models were developed by combining biomarkers and clinical variables in logistic regression models. Accuracy was evaluated with receiver operating characteristic curves. RESULTS: From August 2012 to December 2013, 1308 patients were included (71.9% ischemic, 14.8% stroke mimics, and 13.3% hemorrhagic). For stroke versus stroke mimics comparison, no biomarker resulted included in the logistic regression model, but it was only integrated by clinical variables, with a predictive accuracy of 80.8%. For ischemic versus hemorrhagic strokes comparison, NT-proBNP (N-Terminal Pro-B-Type Natriuretic Peptide) >4.9 (odds ratio, 2.40; 95% confidence interval, 1.55-3.71; <0.0001) and endostatin >4.7 (odds ratio, 2.02; 95% confidence interval, 1.19-3.45; =0.010), together with age, sex, blood pressure, stroke severity, atrial fibrillation, and hypertension, were included in the model. Predictive accuracy was 80.6%. CONCLUSIONS: The studied biomarkers were not sufficient for an accurate differential diagnosis of stroke in the hyperacute setting. Additional discovery of new biomarkers and improvement on laboratory techniques seem necessary for achieving a molecular diagnosis of stroke.
Tipo de publicação: JOURNAL ARTICLE; OBSERVATIONAL STUDY
Nome de substância:0 (Apolipoprotein C-III); 0 (Biomarkers); 0 (Cell Adhesion Molecules); 0 (Chemokine CXCL1); 0 (Endostatins); 0 (FASLG protein, human); 0 (Fas Ligand Protein); 0 (Fibrin Fibrinogen Degradation Products); 0 (Fibronectins); 0 (HSC70 Heat-Shock Proteins); 0 (HSPA8 protein, human); 0 (IGFBP3 protein, human); 0 (IL17A protein, human); 0 (IL2RG protein, human); 0 (IL6 protein, human); 0 (Insulin-Like Growth Factor Binding Protein 3); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-17); 0 (Interleukin-6); 0 (NGF protein, human); 0 (Neural Cell Adhesion Molecules); 0 (Peptide Fragments); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (S100 Calcium Binding Protein beta Subunit); 0 (S100B protein, human); 0 (fibrin fragment D); 0 (pro-brain natriuretic peptide (1-76)); 0 (von Willebrand Factor); 114471-18-0 (Natriuretic Peptide, Brain); 9061-61-4 (Nerve Growth Factor); EC 1.4.3.21 (AOC3 protein, human); EC 1.4.3.21 (Amine Oxidase (Copper-Containing)); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 4.2.1.11 (Phosphopyruvate Hydratase)


  4 / 637 MEDLINE  
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PMID:28687660
Autor:Resende M; Cardoso MS; Ribeiro AR; Flórido M; Borges M; Castro AG; Alves NL; Cooper AM; Appelberg R
Endereço:IBMC - Instituto de Biologia Molecular e Celular and i3S - Instituto de Investigação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal; mrsilva@ibmc.up.pt.
Título:Innate IFN-γ-Producing Cells Developing in the Absence of IL-2 Receptor Common γ-Chain.
Fonte:J Immunol; 199(4):1429-1439, 2017 Aug 15.
ISSN:1550-6606
País de publicação:United States
Idioma:eng
Resumo:IFN-γ is known to be predominantly produced by lymphoid cells such as certain subsets of T cells, NK cells, and other group 1 innate lymphoid cells. In this study, we used IFN-γ reporter mouse models to search for additional cells capable of secreting this cytokine. We identified a novel and rare population of nonconventional IFN-γ-producing cells of hematopoietic origin that were characterized by the expression of Thy1.2 and the lack of lymphoid, myeloid, and NK lineage markers. The expression of IFN-γ by this population was higher in the liver and lower in the spleen. Furthermore, these cells were present in mice lacking both the and the common γ-chain (γc) genes (Rag2 γc ), indicating their innate nature and their γc cytokine independence. Rag2 γc mice are as resistant to as Rag2 mice, whereas Rag2 mice lacking IFN-γ are more susceptible than either or Rag2 γc These lineage-negative CD45 /Thy1.2 cells are found within the mycobacterially induced granulomatous structure in the livers of infected Rag2 γc animals and are adjacent to macrophages that expressed inducible NO synthase, suggesting a potential protective role for these IFN-γ-producing cells. Accordingly, Thy1.2-specific mAb administration to infected Rag2 γc animals increased growth in the liver. Overall, our results demonstrate that a population of Thy1.2 non-NK innate-like cells present in the liver expresses IFN-γ and can confer protection against infection in immunocompromised mice.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antibodies, Monoclonal); 0 (DNA-Binding Proteins); 0 (Interleukin Receptor Common gamma Subunit); 0 (Rag2 protein, mouse); 0 (Thy-1 Antigens); 82115-62-6 (Interferon-gamma); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse); EC 3.1.3.48 (Leukocyte Common Antigens); EC 3.1.3.48 (Ptprc protein, mouse)


  5 / 637 MEDLINE  
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PMID:28678791
Autor:Charych D; Khalili S; Dixit V; Kirk P; Chang T; Langowski J; Rubas W; Doberstein SK; Eldon M; Hoch U; Zalevsky J
Endereço:Nektar Therapeutics, San Francisco, California, United States of America.
Título:Modeling the receptor pharmacology, pharmacokinetics, and pharmacodynamics of NKTR-214, a kinetically-controlled interleukin-2 (IL2) receptor agonist for cancer immunotherapy.
Fonte:PLoS One; 12(7):e0179431, 2017.
ISSN:1932-6203
País de publicação:United States
Idioma:eng
Resumo:Cytokines are potent immune modulating agents but are not ideal medicines in their natural form due to their short half-life and pleiotropic systemic effects. NKTR-214 is a clinical-stage biologic that comprises interleukin-2 (IL2) protein bound by multiple releasable polyethylene glycol (PEG) chains. In this highly PEG-bound form, the IL2 is inactive; therefore, NKTR-214 is a biologic prodrug. When administered in vivo, the PEG chains slowly release, creating a cascade of increasingly active IL2 protein conjugates bound by fewer PEG chains. The 1-PEG-IL2 and 2-PEG-IL2 species derived from NKTR-214 are the most active conjugated-IL2 species. Free-IL2 protein is undetectable in vivo as it is eliminated faster than formed. The PEG chains on NKTR-214 are located at the region of IL2 that contacts the alpha (α) subunit of the heterotrimeric IL2 receptor complex, IL2Rαßγ, reducing its ability to bind and activate the heterotrimer. The IL2Rαßγ complex is constitutively expressed on regulatory T cells (Tregs). Therefore, without the use of mutations, PEGylation reduces the affinity for IL2Rαßγ to a greater extent than for IL2Rßγ, the receptor complex predominant on CD8 T cells. NKTR-214 treatment in vivo favors activation of CD8 T cells over Tregs in the tumor microenvironment to provide anti-tumor efficacy in multiple syngeneic models. Mechanistic modeling based on in vitro and in vivo kinetic data provides insight into the mechanism of NKTR-214 pharmacology. The model reveals that conjugated-IL2 protein derived from NKTR-214 occupy IL-2Rßγ to a greater extent compared to free-IL2 protein. The model accurately describes the sustained in vivo signaling observed after a single dose of NKTR-214 and explains how the properties of NKTR-214 impart a unique kinetically-controlled immunological mechanism of action.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-2 Receptor beta Subunit); 0 (NKTR-214); 0 (Prodrugs); 0 (Receptors, Interleukin-2); 0 (STAT5 Transcription Factor); 30IQX730WE (Polyethylene Glycols)


  6 / 637 MEDLINE  
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PMID:28678090
Autor:Shigemura T; Motobayashi M; Matsuda K; Shimodaira T; Kurata T; Kobayashi N; Agematsu K; Nakazawa Y
Endereço:*Department of Pediatrics, Shinshu University School of Medicine †Department of Laboratory Medicine, Shinshu University Hospital ‡Department of Infection and Host Defense, Graduate School of Medicine, Shinshu University, Matsumoto, Japan.
Título:Acute Myeloid Leukemia in a Patient With X-linked Severe Combined Immunodeficiency.
Fonte:J Pediatr Hematol Oncol; 39(8):e470-e472, 2017 Nov.
ISSN:1536-3678
País de publicação:United States
Idioma:eng
Resumo:Severe combined immunodeficiency (SCID) is a defect in the differentiation and function of T cells. An increased malignancy risk, mainly lymphatic malignancy, has been described in patients with SCID. We report a patient with X-linked SCID who developed acute myeloid leukemia, derived from the recipient with somatic NRAS mutation 4 months after cord blood transplantation (CBT). Loss of heterozygosity phenomenon of the recipient at 6q14 locus was observed at 2 months post-CBT and progressed to 6q deletion (6q-) chromosome abnormality. Somatic NRAS mutation was detected at 3 months post-CBT. Thus, 6q- and NRAS mutation were strongly associated with the leukemic transformation in our patient.
Tipo de publicação: CASE REPORTS; JOURNAL ARTICLE
Nome de substância:0 (IL2RG protein, human); 0 (Immunosuppressive Agents); 0 (Interleukin Receptor Common gamma Subunit)


  7 / 637 MEDLINE  
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PMID:28665482
Autor:Geraghty NJ; Belfiore L; Ly D; Adhikary SR; Fuller SJ; Varikatt W; Sanderson-Smith ML; Sluyter V; Alexander SI; Sluyter R; Watson D
Endereço:School of Biological Sciences, University of Wollongong, Wollongong, NSW, Australia.
Título:The P2X7 receptor antagonist Brilliant Blue G reduces serum human interferon-γ in a humanized mouse model of graft-versus-host disease.
Fonte:Clin Exp Immunol; 190(1):79-95, 2017 Oct.
ISSN:1365-2249
País de publicação:England
Idioma:eng
Resumo:Graft-versus-host disease (GVHD) remains a major problem after allogeneic haematopoietic stem cell transplantation, a curative therapy for haematological malignancies. Previous studies have demonstrated a role for the adenosine triphosphate (ATP)-gated P2X7 receptor channel in allogeneic mouse models of GVHD. In this study, injection of human peripheral blood mononuclear cells (PBMCs) into immunodeficient non-obese diabetic-severe combined immunodeficiency-interleukin (NOD-SCID-IL)-2Rγ (NSG) mice established a humanized mouse model of GVHD. This model was used to study the effect of P2X7 blockade in this disease. From five weeks post-PBMC injection, humanized mice exhibited clinical signs and histopathology characteristic of GVHD. The P2X7 antagonist, Brilliant Blue G (BBG), blocked ATP-induced cation uptake into both murine and human cells in vitro. Injection of BBG (50 mg/kg) into NSG mice did not affect engraftment of human leucocytes (predominantly T cells), or the clinical score and survival of mice. In contrast, BBG injection reduced circulating human interferon (IFN)-γ significantly, which was produced by human CD4 and CD8 T cells. BBG also reduced human T cell infiltration and apoptosis in target organs of GVHD. In conclusion, the P2X7 antagonist BBG reduced circulating IFN-γ in a humanized mouse model of GVHD supporting a potential role for P2X7 to alter the pathology of this disease in humans.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit); 0 (Purinergic P2X Receptor Antagonists); 0 (Receptors, Purinergic P2X7); 0 (Rosaniline Dyes); 82115-62-6 (Interferon-gamma); M1ZRX790SI (coomassie Brilliant Blue)


  8 / 637 MEDLINE  
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PMID:28572216
Autor:Giessler KM; Kleinheinz K; Huebschmann D; Balasubramanian GP; Dubash TD; Dieter SM; Siegl C; Herbst F; Weber S; Hoffmann CM; Fronza R; Buchhalter I; Paramasivam N; Eils R; Schmidt M; von Kalle C; Schneider M; Ulrich A; Scholl C; Fröhling S; Weichert W; Brors B; Schlesner M; Ball CR; Glimm H
Endereço:Department of Translational Oncology, National Center for Tumor Diseases and German Cancer Research Center, Heidelberg, Germany.
Título:Genetic subclone architecture of tumor clone-initiating cells in colorectal cancer.
Fonte:J Exp Med; 214(7):2073-2088, 2017 Jul 03.
ISSN:1540-9538
País de publicação:United States
Idioma:eng
Resumo:A hierarchically organized cell compartment drives colorectal cancer (CRC) progression. Genetic barcoding allows monitoring of the clonal output of tumorigenic cells without prospective isolation. In this study, we asked whether tumor clone-initiating cells (TcICs) were genetically heterogeneous and whether differences in self-renewal and activation reflected differential kinetics among individual subclones or functional hierarchies within subclones. Monitoring genomic subclone kinetics in three patient tumors and corresponding serial xenografts and spheroids by high-coverage whole-genome sequencing, clustering of genetic aberrations, subclone combinatorics, and mutational signature analysis revealed at least two to four genetic subclones per sample. Long-term growth in serial xenografts and spheroids was driven by multiple genomic subclones with profoundly differing growth dynamics and hence different quantitative contributions over time. Strikingly, genetic barcoding demonstrated stable functional heterogeneity of CRC TcICs during serial xenografting despite near-complete changes in genomic subclone contribution. This demonstrates that functional heterogeneity is, at least frequently, present within genomic subclones and independent of mutational subclone differences.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit)


  9 / 637 MEDLINE  
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PMID:28527810
Autor:Nowlan B; Futrega K; Brunck ME; Walkinshaw G; Flippin LE; Doran MR; Levesque JP
Endereço:Stem Cell Therapies Laboratory, Translational Research Institute, Queensland University of Technology, Woolloongabba, Queensland, Australia; Mater Research Institute, Translational Research Institute, University of Queensland, Woolloongabba, Queensland, Australia.
Título:HIF-1α-stabilizing agent FG-4497 rescues human CD34 cell mobilization in response to G-CSF in immunodeficient mice.
Fonte:Exp Hematol; 52:50-55.e6, 2017 Aug.
ISSN:1873-2399
País de publicação:Netherlands
Idioma:eng
Resumo:Granulocyte colony-stimulating factor (G-CSF) is used routinely in the clinical setting to mobilize hematopoietic stem progenitor cells (HSPCs) into the patient's blood for collection and subsequent transplantation. However, a significant proportion of patients who have previously received chemotherapy or radiotherapy and require autologous HSPC transplantation cannot mobilize the minimal threshold of mobilized HSPCs to achieve rapid and successful hematopoietic reconstitution. Although several alternatives to the G-CSF regime have been tested, few are used in the clinical setting. We have shown previously in mice that administration of prolyl 4-hydroxylase domain enzyme (PHD) inhibitors, which stabilize hypoxia-inducible factor (HIF)-1α, synergize with G-CSF in vivo to enhance mouse HSPC mobilization into blood, leading to enhanced engraftment via an HSPC-intrinsic mechanism. To evaluate whether PHD inhibitors could be used to enhance mobilization of human HSPCs, we humanized nonobese, diabetic severe combined immune-deficient Il2rg mice by transplanting them with human umbilical cord blood CD34 HSPCs and then treating them with G-CSF with and without co-administration of the PHD inhibitor FG-4497. We observed that combination treatment with G-CSF and FG-4497 resulted in significant mobilization of human lineage-negative (Lin ) CD34 HSPCs and more primitive human Lin CD34 CD38 HSPCs into blood and spleen, whereas mice treated with G-CSF alone did not mobilize human HSPCs significantly. These results suggest that the PHD inhibitor FG-4497 also increases human HSPC mobilization in a xenograft mouse model, suggesting the possibility of testing PHD inhibitors to boost HSPC mobilization in response to G-CSF in humans.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antigens, CD34); 0 (FG-4497); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit); 0 (Isoquinolines); 0 (Prolyl-Hydroxylase Inhibitors); 143011-72-7 (Granulocyte Colony-Stimulating Factor)


  10 / 637 MEDLINE  
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PMID:28507024
Autor:Meghnem D; Morisseau S; Frutoso M; Trillet K; Maillasson M; Barbieux I; Khaddage S; Leray I; Hildinger M; Quéméner A; Jacques Y; Mortier E
Endereço:Centre de Recherche en Cancérologie et Immunologie Nantes-Angers, CNRS, Inserm, Université de Nantes, Nantes 44007, France.
Título:Cutting Edge: Differential Fine-Tuning of IL-2- and IL-15-Dependent Functions by Targeting Their Common IL-2/15Rß/γc Receptor.
Fonte:J Immunol; 198(12):4563-4568, 2017 Jun 15.
ISSN:1550-6606
País de publicação:United States
Idioma:eng
Resumo:Interleukin 2 and IL-15 are two closely related cytokines, displaying important functions in the immune system. They share the heterodimeric CD122/CD132 receptor to deliver their signals within target cells. Their specificity of action is conferred by their α receptor chains, IL-2Rα and IL-15Rα. By combining an increased affinity for CD122 and an impaired recruitment of CD132, we have generated an original molecule named IL-2Rß/γ (CD122/CD132) inhibitor (BiG), targeting the CD122/CD132 receptor. BiG efficiently inhibited IL-15- and IL-2-dependent functions of primary cells, including CD8 T and NK cells, in vitro and in vivo. We also report a differential dynamic of action of these cytokines by highlighting a major role played by the IL-2Rα receptor. Interestingly, due to the presence of IL-2Rα, BiG had no impact on IL-2-dependent regulatory T cell proliferation. Thus, by acting as a fine switch in the immune system, BiG emphasizes the differential roles of these two cytokines.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (IL2RA protein, human); 0 (IL2RB protein, human); 0 (IL2RG protein, human); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-15); 0 (Interleukin-15 Receptor alpha Subunit); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-2 Receptor beta Subunit)



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