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[PMID]: 29412476
[Au] Autor:Bakela K; Dimakopoulou M; Batsou P; Manidakis N; Athanassakis I
[Ad] Address:Laboratory of Immunology, Department of Biology, University of Crete, Heraklion, Crete, Greece.
[Ti] Title:Soluble MHC class II-driven therapy for a systemic lupus erythematosus murine experimental in vitro and in vivo model.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Taking into consideration the multiparametric nature of systemic lupus erythematosus (SLE), the severity and variability of symptoms and the lack of effective therapeutic approaches, this study took advantage of the recently described role of soluble major histocompatibility complex class II (sMHCII) molecules in maintaining tolerance to the organism and attempted to apply sMHCII proteins as a treatment to murine SLE experimental models in vitro as well as in vivo. After breaking tolerance to DNA in vitro, which was accompanied by development of specific anti-dsDNA antibodies, syngeneic or allogeneic sMHCII molecules, purified from healthy mouse serum, could significantly reduce the specific antibody levels and drive the system towards immunosuppression, as assessed by specific marker analysis on T cells and cytokine production by flow cytometry and ELISA, respectively. The in vivo experimental model consisted of pristane-induced SLE symptoms to BALB/c mice, which developed maximal levels of anti-dsDNA 2 months after pristane inoculation. Syngeneic or allogeneic sMHCII administration could alleviate pristane-induced symptoms, significantly decrease specific anti-dsDNA antibody production and develop immunosuppression to the host, as manifested by increase of CD4 + CTLA-4 +  and CD4 + CD25 +  cell populations in the spleen. Thus, the results presented in this study introduced the ability of sMHCII proteins to suppress specific autoantigen response, opening new areas of research and offering novel therapeutic approaches to SLE with expanding features to other autoimmune diseases.
[Mh] MeSH terms primary: Antibodies, Antinuclear/immunology
Autoantigens/immunology
Histocompatibility Antigens Class II/immunology
Immune Tolerance/immunology
Immunotherapy/methods
Lupus Erythematosus, Systemic/immunology
Lupus Erythematosus, Systemic/therapy
T-Lymphocytes/immunology
[Mh] MeSH terms secundary: Animals
CD4 Antigens/metabolism
CTLA-4 Antigen/metabolism
Cells, Cultured
DNA/immunology
Disease Models, Animal
Immunosuppression
Interleukin-2 Receptor alpha Subunit/metabolism
Lupus Erythematosus, Systemic/chemically induced
Mice
Mice, Inbred BALB C
Spleen/cytology
Spleen/immunology
Terpenes/adverse effects
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antibodies, Antinuclear); 0 (Autoantigens); 0 (CD4 Antigens); 0 (CTLA-4 Antigen); 0 (Histocompatibility Antigens Class II); 0 (Il2ra protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Terpenes); 26HZV48DT1 (pristane); 9007-49-2 (DNA)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180208
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12644

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[PMID]: 29363337
[Au] Autor:Patti F; Chisari CG; D'Amico E; Zappia M
[Ad] Address:a Department "GF Ingrassia", Section of Neurosciences, Multiple Sclerosis Center , University of Catania , Catania , Italy.
[Ti] Title:Pharmacokinetic drug evaluation of daclizumab for the treatment of relapsing-remitting multiple sclerosis.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):341-352, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. Despite the availability of several disease-modifying therapies for relapsing MS, there is a need for highly efficacious targeted therapy with a favorable benefit-risk profile and a high level of treatment adherence. Daclizumab is a humanized monoclonal antibody directed against CD25, the α subunit of the high-affinity interleukin 2 (IL-2) receptor, that reversibly modulates IL-2 signaling. Areas covered: Daclizumab blocks the activation and expansion of autoreactive T cells that plays a role in the immune pathogenesis of MS. As its modulatory effects on the immune system, daclizumab's potential for use in MS was tested extensively showing a high efficacy in reducing relapse rate, disability progression and the number and volume of gadolinium-enhancing lesions on brain magnetic resonance imaging. Moreover, phase II and III trials showed a favorable pharmacokinetic (PK) profile with slow clearance, linear pharmacokinetics at doses above 100 mg and high subcutaneous bioavailability, not influenced by age, sex or other clinical parameters. Expert opinion: Among the new emerging drugs for MS, daclizumab also, thanks to a favorable PK profile, may represent an interesting and promising therapeutic option in the wide MS therapies armamentarium.
[Mh] MeSH terms primary: Antibodies, Monoclonal, Humanized/administration & dosage
Immunoglobulin G/administration & dosage
Immunosuppressive Agents/administration & dosage
Multiple Sclerosis, Relapsing-Remitting/drug therapy
[Mh] MeSH terms secundary: Animals
Antibodies, Monoclonal, Humanized/pharmacokinetics
Antibodies, Monoclonal, Humanized/pharmacology
Biological Availability
Dose-Response Relationship, Drug
Humans
Immunoglobulin G/pharmacology
Immunosuppressive Agents/pharmacokinetics
Immunosuppressive Agents/pharmacology
Interleukin-2 Receptor alpha Subunit/immunology
Magnetic Resonance Imaging
Medication Adherence
Multiple Sclerosis, Relapsing-Remitting/physiopathology
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Antibodies, Monoclonal, Humanized); 0 (IL2RA protein, human); 0 (Immunoglobulin G); 0 (Immunosuppressive Agents); 0 (Interleukin-2 Receptor alpha Subunit); CUJ2MVI71Y (daclizumab)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180125
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1432594

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[PMID]: 28457753
[Au] Autor:Sadovnik I; Herrmann H; Eisenwort G; Blatt K; Hoermann G; Mueller N; Sperr WR; Valent P
[Ad] Address:Department of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, Vienna, Austria.
[Ti] Title:Expression of CD25 on leukemic stem cells in BCR-ABL1 CML: Potential diagnostic value and functional implications.
[So] Source:Exp Hematol;51:17-24, 2017 07.
[Is] ISSN:1873-2399
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Chronic myeloid leukemia (CML) is a stem cell-derived leukemia in which neoplastic cells exhibit the Philadelphia chromosome and the related oncoprotein BCR-ABL1. The disease is characterized by an accumulation of myeloid precursor cells in the peripheral blood and bone marrow (BM). A small fraction of neoplastic cells in the CML clone supposedly exhibits self-renewal and thus long-term disease-propagating ability. However, so far, little is known about the phenotype, function, and target expression profiles of these leukemic stem cells (LSCs). Recent data suggest that CML LSCs aberrantly express the interleukin-2 receptor alpha chain CD25. Whereas normal CD34 /CD38 BM stem cells display only low amounts of CD25 or lack CD25 altogether, CD34 /CD38 LSCs express CD25 strongly in more than 90% of all patients with untreated CML. As a result, CD25 can be used to identify and quantify CML LSCs. In addition, it has been shown that CD25 serves as a negative growth regulator of CML LSCs. Here, we review the value of CD25 as a novel marker and potential drug target in CML LSCs.
[Mh] MeSH terms primary: Biomarkers, Tumor/biosynthesis
Fusion Proteins, bcr-abl/metabolism
Gene Expression Regulation, Leukemic
Interleukin-2 Receptor alpha Subunit/biosynthesis
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism
Neoplasm Proteins/metabolism
Neoplastic Stem Cells/metabolism
[Mh] MeSH terms secundary: ADP-ribosyl Cyclase 1/metabolism
Antigens, CD34/metabolism
Bone Marrow Cells/metabolism
Humans
Membrane Glycoproteins/metabolism
Neoplastic Stem Cells/pathology
[Pt] Publication type:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antigens, CD34); 0 (BCR-ABL1 fusion protein, human); 0 (Biomarkers, Tumor); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Membrane Glycoproteins); 0 (Neoplasm Proteins); EC 2.7.10.2 (Fusion Proteins, bcr-abl); EC 3.2.2.5 (CD38 protein, human); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Entry month:1709
[Cu] Class update date: 180224
[Lr] Last revision date:180224
[Js] Journal subset:IM
[Da] Date of entry for processing:170502
[St] Status:MEDLINE

  4 / 5301 MEDLINE  
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[PMID]: 29307521
[Au] Autor:Han W; Ni Q; Liu K; Yao Y; Zhao D; Liu X; Chen Y
[Ad] Address:Department of Laboratory Medicine, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou 310003, China; Key Laboratory of Clinical In Vitro Diagnostic Techniques of Zhejiang Province, 79 Qingchun Road, Hangzhou 310003, China.
[Ti] Title:Decreased CD122 on CD56 NK associated with its impairment in asymptomatic chronic HBV carriers with high levels of HBV DNA, HBsAg and HBeAg.
[So] Source:Life Sci;195:53-60, 2018 Feb 15.
[Is] ISSN:1879-0631
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:AIMS: NK cells play important roles in inhibiting HBV replication and preventing HBV infection. However, NK-cell dysfunction has not been fully studied in asymptomatic chronic HBV carriers (ASC). This study aims to assess decreased expression of CD122 associated with impaired NK cells and the restoration of NK cells with IL-2 and IL-15 stimulation. MAIN METHODS: The experiments were performed by flow cytometer, cytotoxicity assay, ELISA and western blotting. KEY FINDINGS: The reduced CD122 on CD56 NK cells and CD56 NK cells is associated with high levels of HBV DNA, HBsAg or HBeAg in ASCs, in which CD56 NK-cell impairment is observed. Moreover, decreased IFN-γ and degranulation and low cytotoxicity by CD56 NK cells after CD122 blockade were revealed. IL-2 and/or IL-15 can restore impaired CD56 NK cells, together with increased p-STAT5, which can be reversed by CD122 blockade. Additionally, IL-2 or IL-15 can enhance IFN-α2-activated CD56 NK-cell immune responses via up-regulating interferon alpha and beta receptor subunit 2 (IFNAR2). SIGNIFICANCE: Down-regulated CD122 on CD56 NK cell in ASCs with massive viral antigens and high viremia is associated with its impairment, which can be restored by IL-2 and/or IL-15, or combined with IFN-α2.
[Mh] MeSH terms primary: CD56 Antigen/biosynthesis
DNA, Viral/biosynthesis
Hepatitis B Surface Antigens/blood
Hepatitis B e Antigens/blood
Hepatitis B virus/metabolism
Hepatitis B/metabolism
Interleukin-2 Receptor beta Subunit/biosynthesis
Killer Cells, Natural/metabolism
[Mh] MeSH terms secundary: Adult
CD56 Antigen/genetics
Carrier State
DNA, Viral/genetics
Female
Hepatitis B virus/genetics
Humans
Interferon-gamma/biosynthesis
Interleukin-15/pharmacology
Interleukin-2/pharmacology
Interleukin-2 Receptor beta Subunit/genetics
Male
Receptor, Interferon alpha-beta/biosynthesis
Receptor, Interferon alpha-beta/genetics
STAT5 Transcription Factor/biosynthesis
STAT5 Transcription Factor/genetics
Viremia/blood
Viremia/virology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (CD56 Antigen); 0 (DNA, Viral); 0 (Hepatitis B Surface Antigens); 0 (Hepatitis B e Antigens); 0 (IFNAR2 protein, human); 0 (Interleukin-15); 0 (Interleukin-2); 0 (Interleukin-2 Receptor beta Subunit); 0 (STAT5 Transcription Factor); 156986-95-7 (Receptor, Interferon alpha-beta); 82115-62-6 (Interferon-gamma)
[Em] Entry month:1802
[Cu] Class update date: 180208
[Lr] Last revision date:180208
[Js] Journal subset:IM
[Da] Date of entry for processing:180109
[St] Status:MEDLINE

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[PMID]: 29261670
[Au] Autor:Jeffery HC; McDowell P; Lutz P; Wawman RE; Roberts S; Bagnall C; Birtwistle J; Adams DH; Oo YH
[Ad] Address:Centre for Liver Research and National Institute for Health Research Birmingham Biomedical Research Centre, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
[Ti] Title:Human intrahepatic ILC2 are IL-13positive amphiregulinpositive and their frequency correlates with model of end stage liver disease score.
[So] Source:PLoS One;12(12):e0188649, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Innate lymphoid cells (ILC) have been implicated in the initiation of inflammation and fibrosis in mice. However, ILC have not been characterized in inflamed human liver tissue. METHODS: Human intrahepatic lymphocytes were isolated by mechanical digestion and phenotyped by flow cytometry. Conditioned medium from cultures of primary human biliary epithelial cells, stellate cells, fibroblasts and inflamed human liver tissue was used to model the effects of the inflammatory liver environment of ILC phenotype and function. RESULTS: All three ILC subsets were present in the human liver, with the ILC1 (CRTH2negCD117neg) subset constituting around 70% of intrahepatic ILCs. Both NCRpos (NKp44+) and NCRneg ILC3 (CRTH2negCD117pos) subsets were also detected. ILC2 (CRTH2pos) frequency correlated with disease severity measured by model of end stage liver disease (MELD) scoring leading us to study this subset in more detail. ILC2 displayed a tissue resident CD69+ CD161++ phenotype and expressed chemokine receptor CCR6 allowing them to respond to CCL20 secreted by cholangiocytes and stellate cells. ILC2 expressed integrins VLA-5 and VLA-6 and the IL-2 and IL-7 cytokine receptors CD25 and CD127 although IL-2 and IL-7 were barely detectable in inflamed liver tissue. Although biliary epithelial cells secrete IL-33, intrahepatic ILC2 had low expression of the ST2 receptor. Intrahepatic ILC2 secreted the immunoregulatory and repair cytokines IL-13 and amphiregulin. CONCLUSIONS: Intrahepatic ILC2 express receptors allowing them to be recruited to bile ducts in inflamed portal tracts. Their frequencies increased with worsening liver function. Their secretion of IL-13 and amphiregulin suggests they may be recruited to promote resolution and repair and thereby they may contribute to ongoing fibrogenesis in liver disease.
[Mh] MeSH terms primary: Amphiregulin/metabolism
End Stage Liver Disease/immunology
Immunity, Innate
Interleukin-13/metabolism
Liver/metabolism
Lymphocytes/metabolism
Models, Biological
[Mh] MeSH terms secundary: Epithelial Cells/metabolism
Humans
Inflammation/pathology
Integrins/genetics
Integrins/metabolism
Interleukin-2/metabolism
Interleukin-2 Receptor alpha Subunit/metabolism
Interleukin-7/metabolism
Liver/pathology
Lymphocyte Count
NK Cell Lectin-Like Receptor Subfamily B/metabolism
Phenotype
Receptors, Chemokine/genetics
Receptors, Chemokine/metabolism
Receptors, Immunologic/metabolism
Receptors, Prostaglandin/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Amphiregulin); 0 (Integrins); 0 (Interleukin-13); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-7); 0 (NK Cell Lectin-Like Receptor Subfamily B); 0 (Receptors, Chemokine); 0 (Receptors, Immunologic); 0 (Receptors, Prostaglandin); 0 (prostaglandin D2 receptor)
[Em] Entry month:1801
[Cu] Class update date: 180108
[Lr] Last revision date:180108
[Js] Journal subset:IM
[Da] Date of entry for processing:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188649

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[PMID]: 29246441
[Au] Autor:Essig K; Hu D; Guimaraes JC; Alterauge D; Edelmann S; Raj T; Kranich J; Behrens G; Heiseke A; Floess S; Klein J; Maiser A; Marschall S; Hrabe de Angelis M; Leonhardt H; Calkhoven CF; Noessner E; Brocker T; Huehn J; Krug AB; Zavolan M; Baumjohann D; Heissmeyer V
[Ad] Address:Institute for Immunology, Biomedical Center, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany.
[Ti] Title:Roquin Suppresses the PI3K-mTOR Signaling Pathway to Inhibit T Helper Cell Differentiation and Conversion of Treg to Tfr Cells.
[So] Source:Immunity;47(6):1067-1082.e12, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Roquin proteins preclude spontaneous T cell activation and aberrant differentiation of T follicular helper (Tfh) or T helper 17 (Th17) cells. Here we showed that deletion of Roquin-encoding alleles specifically in regulatory T (Treg) cells also caused the activation of conventional T cells. Roquin-deficient Treg cells downregulated CD25, acquired a follicular Treg (Tfr) cell phenotype, and suppressed germinal center reactions but could not protect from colitis. Roquin inhibited the PI3K-mTOR signaling pathway by upregulation of Pten through interfering with miR-17∼92 binding to an overlapping cis-element in the Pten 3' UTR, and downregulated the Foxo1-specific E3 ubiquitin ligase Itch. Loss of Roquin enhanced Akt-mTOR signaling and protein synthesis, whereas inhibition of PI3K or mTOR in Roquin-deficient T cells corrected enhanced Tfh and Th17 or reduced iTreg cell differentiation. Thereby, Roquin-mediated control of PI3K-mTOR signaling prevents autoimmunity by restraining activation and differentiation of conventional T cells and specialization of Treg cells.
[Mh] MeSH terms primary: Colitis/immunology
Phosphatidylinositol 3-Kinases/immunology
Repressor Proteins/immunology
TOR Serine-Threonine Kinases/immunology
Ubiquitin-Protein Ligases/immunology
[Mh] MeSH terms secundary: Animals
B-Lymphocytes/immunology
B-Lymphocytes/pathology
Cell Differentiation
Colitis/genetics
Colitis/pathology
Disease Models, Animal
Female
Forkhead Box Protein O1/genetics
Forkhead Box Protein O1/immunology
Gene Expression Regulation
Germinal Center/immunology
Germinal Center/pathology
Interleukin-2 Receptor alpha Subunit/genetics
Interleukin-2 Receptor alpha Subunit/immunology
Lymphocyte Activation
Mice
Mice, Inbred C57BL
Mice, Transgenic
MicroRNAs/genetics
MicroRNAs/immunology
PTEN Phosphohydrolase/genetics
PTEN Phosphohydrolase/immunology
Phosphatidylinositol 3-Kinases/genetics
Primary Cell Culture
Repressor Proteins/deficiency
Repressor Proteins/genetics
Signal Transduction
Spleen/immunology
Spleen/pathology
T-Lymphocytes, Regulatory/immunology
T-Lymphocytes, Regulatory/pathology
TOR Serine-Threonine Kinases/genetics
Th17 Cells/immunology
Th17 Cells/pathology
Ubiquitin-Protein Ligases/deficiency
Ubiquitin-Protein Ligases/genetics
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Forkhead Box Protein O1); 0 (Foxo1 protein, mouse); 0 (Il2ra protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 0 (MIRN17-92 microRNA, mouse); 0 (MicroRNAs); 0 (Repressor Proteins); 0 (roquin-2 protein, mouse); EC 2.3.2.26 (Itch protein, mouse); EC 2.3.2.27 (Rc3h1 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.1.1 (mTOR protein, mouse); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (Pten protein, mouse)
[Em] Entry month:1712
[Cu] Class update date: 171226
[Lr] Last revision date:171226
[Js] Journal subset:IM
[Da] Date of entry for processing:171217
[St] Status:MEDLINE

  7 / 5301 MEDLINE  
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[PMID]: 29246655
[Au] Autor:Hosseinian H; Mahnam K; Shakhsi-Niaei M
[Ad] Address:Departments of Genetics, Faculty of Science, Shahrekord University, Shahrekord, Iran.
[Ti] Title:The c.305del3 in IL-2 gene in Homonoidea theoretically affects IL-2/IL-2Rα interaction as well as lymphocyte homeostasis.
[So] Source:Cytokine;, 2017 Dec 12.
[Is] ISSN:1096-0023
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Interleukin-2 (IL-2) is a well-known monomeric T-cell growth factor that is produced primarily by activated CD4+ T cells following exposure to antigen. IL-2 structural analysis among primates showed a few polymorphisms as well as a 3-nucleotide deletion (c.305del3) in Hominoidea superfamily including Homo sapiens. On the other hand, the interaction of IL-2 with its alpha subunit of the receptor (IL-2Rα) is the first step for assembly of the whole IL-2R and considered as a species-specific phase. Four models of human IL-2, IL-2Rα, and their ancestral forms were made and were used for molecular dynamics (MD) simulation. Subsequently, the final structures were docked to each other and finally, the complexes were used for MD simulation. Our results showed that the above mentioned deletion led to weaker interaction of human IL-2 to its receptor relative toancestral IL-2. Association study of lymphocyte counts, as an indicator of IL-2 function, in 78 primate species with or without this deletion showed significant association of this deletion with their overall lymphocyte counts (P < .01). Therefore, it can be suggested that p.81delThr in IL-2 in Hominides superfamily interfered with interaction of IL-2 and IL-2Rα and led to overall decrease in lymphocyte counts in this superfamily of primates in comparison with other primates.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 171216
[Lr] Last revision date:171216
[St] Status:Publisher

  8 / 5301 MEDLINE  
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[PMID]: 29045900
[Au] 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
[Ad] Address:INSERM U1126, Université Paris-Diderot, École Pratique des Hautes Etudes/PSL Research University, Institut Universitaire d'Hématologie, Hôpital Saint-Louis, Paris, France.
[Ti] Title:Molecular and Functional Characterization of Lymphoid Progenitor Subsets Reveals a Bipartite Architecture of Human Lymphopoiesis.
[So] Source:Immunity;47(4):680-696.e8, 2017 Oct 17.
[Is] ISSN:1097-4180
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract: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.
[Mh] MeSH terms primary: B-Lymphocytes/metabolism
Killer Cells, Natural/metabolism
Lymphoid Progenitor Cells/metabolism
Lymphopoiesis/genetics
T-Lymphocytes/metabolism
[Mh] MeSH terms secundary: Adolescent
Adult
Animals
B-Lymphocytes/cytology
Cell Differentiation/genetics
Cell Lineage/genetics
Cells, Cultured
Female
Gene Expression Profiling/methods
Humans
Interleukin Receptor Common gamma Subunit/deficiency
Interleukin Receptor Common gamma Subunit/genetics
Interleukin-7 Receptor alpha Subunit/genetics
Interleukin-7 Receptor alpha Subunit/metabolism
Killer Cells, Natural/cytology
Lymphoid Progenitor Cells/cytology
Lymphoid Progenitor Cells/transplantation
Male
Mice, Inbred NOD
Mice, Knockout
Mice, SCID
Middle Aged
Stem Cell Transplantation
T-Lymphocytes/cytology
Transplantation, Heterologous
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-7 Receptor alpha Subunit)
[Em] Entry month:1711
[Cu] Class update date: 171106
[Lr] Last revision date:171106
[Js] Journal subset:IM
[Da] Date of entry for processing:171019
[St] Status:MEDLINE

  9 / 5301 MEDLINE  
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[PMID]: 28942020
[Au] Autor:Lang C; Wang J; Chen L
[Ad] Address:Department of Gastroenterology, Liaocheng People's Hospital, Liaocheng, Shandong Province 252000, China. Electronic address: cuicuilang@163.com.
[Ti] Title:CD25-expressing Th17 cells mediate CD8 T cell suppression in CTLA-4 dependent mechanisms in pancreatic ductal adenocarcinoma.
[So] Source:Exp Cell Res;360(2):384-389, 2017 Nov 15.
[Is] ISSN:1090-2422
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The tumor-associated immune response is governed by the signalling events of various regulatory molecules, one of which is the cytotoxic T lymphocyte-associated antigen 4 (CTLA-4). In conventional T cells, CTLA-4 could outcompete CD28 in binding to CD80/86 but does not produce a co-stimulatory signal, resulting in T cell anergy. CTLA-4 in regulatory T cells (Tregs) could also function in a cell-extrinsic fashion by removing CD80/CD86 from the antigen-presenting cells (APCs), thus preventing further priming of other T cells. In this study, we examined the role of CTLA-4 in CD4 T cell subsets from pancreatic cancer patients. In circulating CD4 T cells, the expression of CTLA-4 was low at baseline but was significantly upregulated following T cell stimulation. Interestingly, the CTLA-4-expressing CD4 T cells at baseline were overwhelmingly FOXP3-expressing. With the increase of T cell stimulation, the proportion of ROR gamma t-expressing CD4 T cells was progressively increased. By CD25 vs. CCR6 staining, the CD25 CCR6 and the CD25 CCR6 CD4 T cells both presented high levels of CTLA-4 expression, but only the CD25 CCR6 and the CD25 CCR6 expressed significant amounts of IL-17. When incubated with autologous CD8 T cells, the CD25 CCR6 Th17 cells presented significantly higher suppressive function than the CD25 CCR6 Th17 cells in a CTLA-4-dependent manner. Finally, the CTLA-4-expressing Th17 cells were present at higher levels in the tumor-infiltrating lymphocytes than in circulating blood. Overall, these data suggest that CTLA-4 expressing Th17 cells may present regulatory activities in pancreatic cancer patients.
[Mh] MeSH terms primary: CD8-Positive T-Lymphocytes/immunology
CTLA-4 Antigen/physiology
Carcinoma, Pancreatic Ductal/immunology
Immune Tolerance
Interleukin-2 Receptor alpha Subunit/metabolism
Pancreatic Neoplasms/immunology
Th17 Cells/immunology
Th17 Cells/metabolism
[Mh] MeSH terms secundary: CD4-Positive T-Lymphocytes/immunology
CD8-Positive T-Lymphocytes/physiology
CTLA-4 Antigen/metabolism
Carcinoma, Pancreatic Ductal/metabolism
Carcinoma, Pancreatic Ductal/pathology
Cell Proliferation
Cells, Cultured
Humans
Interferon-gamma/metabolism
Lymphocyte Activation
Pancreatic Neoplasms/metabolism
Pancreatic Neoplasms/pathology
T-Lymphocytes, Regulatory/immunology
T-Lymphocytes, Regulatory/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (CTLA-4 Antigen); 0 (CTLA4 protein, human); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit); 82115-62-6 (Interferon-gamma)
[Em] Entry month:1711
[Cu] Class update date: 171107
[Lr] Last revision date:171107
[Js] Journal subset:IM
[Da] Date of entry for processing:170925
[St] Status:MEDLINE

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[PMID]: 28935468
[Au] Autor:Ma QY; Huang DY; Zhang HJ; Wang S; Chen XF
[Ad] Address:Department of Thoracic Surgery, Huashan Hospital Affiliated to Fudan University, Shanghai, China.
[Ti] Title:Function and regulation of LAG3 on CD4 CD25 T cells in non-small cell lung cancer.
[So] Source:Exp Cell Res;360(2):358-364, 2017 Nov 15.
[Is] ISSN:1090-2422
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:LAG3 is a surface molecule found on a subset of immune cells. The precise function of LAG3 appears to be context-dependent. In this study, we investigated the effect of LAG3 on CD4 CD25 T cells from non-small cell lung cancer (NSCLC) patients. We found that in the peripheral blood mononuclear cells of NSCLC patients, LAG3 was significantly increased in CD4 T cells directly ex vivo and primarily in the CD4 CD25 fraction, which was regulated by prolonged TCR stimulation and the presence of IL-27. TCR stimulation also increased CD25 expression, but not Foxp3 expression, in LAG3-expressing CD4 CD25 cells Compared to LAG3-nonexpressing CD4 CD25 cells, LAG3-expressing CD4 CD25 cells presented significantly higher levels of PD1 and TIM3, two inhibitory receptors best described in exhausted CD8 T effector cells. LAG3-expressing CD4 CD25 cells also presented impaired proliferation compared with LAG3-nonexpressing CD4 CD25 cells but could be partially rescued by inhibiting both PD1 and TIM3. Interestingly, CD8 T cells co-incubated with LAG3-expressing CD4 CD25 cells at equal cell numbers demonstrated significantly lower proliferation than CD8 T cells incubated alone. Co-culture with CD8 T cell and LAG3-expressing CD4 CD25 T cell also upregulated soluble IL-10 level in the supernatant, of which the concentration was positively correlated with the number of LAG3-expressing CD4 CD25 T cells. In addition, we found that LAG3-expressing CD4 CD25 T cells infiltrated the resected tumors and were present at higher frequencies of in metastases than in primary tumors. Taken together, these data suggest that LAG3-expressing CD4 CD25 T cells represent another regulatory immune cell type with potential to interfere with anti-tumor immunity.
[Mh] MeSH terms primary: Antigens, CD/physiology
CD4-Positive T-Lymphocytes/metabolism
Carcinoma, Non-Small-Cell Lung/immunology
Interleukin-2 Receptor alpha Subunit/metabolism
Lung Neoplasms/immunology
[Mh] MeSH terms secundary: Adult
Aged
Antigens, CD/metabolism
Carcinoma, Non-Small-Cell Lung/metabolism
Carcinoma, Non-Small-Cell Lung/pathology
Case-Control Studies
Cells, Cultured
Female
Humans
Lung Neoplasms/metabolism
Lung Neoplasms/pathology
Male
Middle Aged
T-Lymphocytes, Regulatory/metabolism
T-Lymphocytes, Regulatory/physiology
Tumor Escape/immunology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antigens, CD); 0 (CD223 antigen); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit)
[Em] Entry month:1711
[Cu] Class update date: 171107
[Lr] Last revision date:171107
[Js] Journal subset:IM
[Da] Date of entry for processing:170923
[St] Status:MEDLINE


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