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[PMID]: 25319394
[Au] Autor:Hasanali ZS; Epner EM; Feith DJ; Loughran TP; Sample CE
[Ad] Address:Department of Microbiology and Immunology, Pennsylvania State University College of Medicine and Penn State Hershey Cancer Institute, Hershey, Pennsylvania....
[Ti] Title:Vorinostat downregulates CD30 and decreases brentuximab vedotin efficacy in human lymphocytes.
[So] Source:Mol Cancer Ther;13(12):2784-92, 2014 Dec.
[Is] ISSN:1538-8514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:With an increasing number of clinical trials looking at combination therapies in cancer, potential drug-drug interactions require particular attention. One such instance is the treatment of CD30(+) tumors after previous vorinostat (SAHA; suberoylanilide hydroxyamic acid) failure with the anti-CD30 antibody-drug conjugate brentuximab vedotin. Using B-, T-, and natural killer (NK)-cell lines in vitro, we demonstrate that SAHA downregulates the expression of CD30 and lowers the efficacy of subsequent brentuximab vedotin treatment if baseline CD30 levels are reduced by 50% or more. Interestingly, low-dose SAHA treatment that maintained 50% or more of basal CD30 expression followed by subsequent treatment with brentuximab vedotin led to enhanced antitumor activity. The downregulation of CD30 was short lived upon SAHA removal, suggesting that allowing SAHA washout may circumvent any interactions with subsequent drug therapies. Our findings confirm the requirement of CD30 for brentuximab vedotin efficacy and suggest that combination treatment with SAHA in CD30(dim) tumors may decrease efficacy. Combination treatment in highly CD30(+) tumors, however, increases efficacy and warrants further consideration as a new treatment paradigm. Mol Cancer Ther; 13(12); 2784-92. ©2014 AACR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1158/1535-7163.MCT-14-0593

  2 / 445370 MEDLINE  
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[PMID]: 25415283
[Au] Autor:Soares KC; Rucki AA; Wu AA; Olino K; Xiao Q; Chai Y; Wamwea A; Bigelow E; Lutz E; Liu L; Yao S; Anders RA; Laheru D; Wolfgang CL; Edil BH; Schulick RD; Jaffee EM; Zheng L
[Ad] Address:Departments of *Oncology #Pathology †Surgery ‡The Sidney Kimmel Cancer Center §The Skip Viragh Center for Pancreatic Cancer Research and Clinical Care ∥The Sol Goldman Pancreatic Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD ¶Amplimmune Inc., Gaithersburg, MD **Department of Surgery, University of Colorado School of Medicine, Aurora, CO.
[Ti] Title:PD-1/PD-L1 Blockade Together With Vaccine Therapy Facilitates Effector T-Cell Infiltration Into Pancreatic Tumors.
[So] Source:J Immunother;38(1):1-11, 2015 Jan.
[Is] ISSN:1537-4513
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pancreatic ductal adenocarcinoma (PDA) has a poor prognosis due to late detection and resistance to conventional therapies. Published studies show that the PDA tumor microenvironment is predominantly infiltrated with immune suppressive cells and signals that if altered, would allow effective immunotherapy. However, single-agent checkpoint inhibitors including agents that alter immune suppressive signals in other human cancers such as cytotoxic T-lymphocyte antigen 4 (CTLA-4), programmed death 1 (PD-1), and its ligand PD-L1, have failed to demonstrate objective responses when given as single agents to PDA patients. We recently reported that inhibition of the CTLA-4 pathway when given together with a T cell inducing vaccine gives objective responses in metastatic PDA patients. In this study, we evaluated blockade of the PD-1/PD-L1 pathway. We found that PD-L1 is weakly expressed at a low frequency in untreated human and murine PDAs but treatment with a granulocyte macrophage colony-stimulating factor secreting PDA vaccine (GVAX) significantly upregulates PD-L1 membranous expression after treatment of tumor-bearing mice. In addition, combination therapy with vaccine and PD-1 antibody blockade improved murine survival compared with PD-1 antibody monotherapy or GVAX therapy alone. Furthermore, PD-1 blockade increased effector CD8 T lymphocytes and tumor-specific interferon-γ production of CD8 T cells in the tumor microenvironment. Immunosuppressive pathways, including regulatory T cells and CTLA-4 expression on T cells were overcome by the addition of vaccine and low-dose cyclophosphamide to PD-1 blockade. Collectively, our study supports combining PD-1 or PD-L1 antibody therapy with a T cell inducing agent for PDA treatment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/CJI.0000000000000062

  3 / 445370 MEDLINE  
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[PMID]: 25385825
[Au] Autor:Mutnal MB; Hu S; Schachtele SJ; Lokensgard JR
[Ad] Address:Neuroimmunology Laboratory, Center for Infectious Diseases and Microbiology Translational Research, Department of Medicine, University of Minnesota, Minneapolis, MN 55455....
[Ti] Title:Infiltrating Regulatory B Cells Control Neuroinflammation following Viral Brain Infection.
[So] Source:J Immunol;193(12):6070-80, 2014 Dec 15.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Previous studies have demonstrated the existence of a subset of B lymphocytes, regulatory B cells (Bregs), which modulate immune function. In this study, in vivo and in vitro experiments were undertaken to elucidate the role of these Bregs in controlling neuroinflammation following viral brain infection. We used multicolor flow cytometry to phenotype lymphocyte subpopulations infiltrating the brain, along with in vitro cocultures to assess their anti-inflammatory and immunoregulatory roles. This distinctive subset of CD19(+)CD1d(hi)CD5(+) B cells was found to infiltrate the brains of chronically infected animals, reaching highest levels at the latest time point tested (30 d postinfection). B cell-deficient Jh(-/-) mice were found to develop exacerbated neuroimmune responses as measured by enhanced accumulation and/or retention of CD8(+) T cells within the brain, as well as increased levels of microglial activation (MHC class II). Conversely, levels of Foxp3(+) regulatory T cells were found to be significantly lower in Jh(-/-) mice when compared with wild-type (Wt) animals. Further experiments showed that in vitro-generated IL-10-secreting Bregs (B10) were able to inhibit cytokine responses from microglia following stimulation with viral Ags. These in vitro-generated B10 cells were also found to promote proliferation of regulatory T cells in coculture studies. Finally, gain-of-function experiments demonstrated that reconstitution of Wt B cells into Jh(-/-) mice restored neuroimmune responses to levels exhibited by infected Wt mice. Taken together, these results demonstrate that Bregs modulate T lymphocyte as well as microglial cell responses within the infected brain and promote CD4(+)Foxp3(+) T cell proliferation in vitro.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1400654

  4 / 445370 MEDLINE  
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[PMID]: 25378593
[Au] Autor:Mikacenic C; Schneider A; Radella F; Buckner JH; Wurfel MM
[Ad] Address:Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, Seattle, WA 98104; and cmikacen@uw.edu....
[Ti] Title:Cutting Edge: Genetic Variation in TLR1 Is Associated with Pam3CSK4-Induced Effector T Cell Resistance to Regulatory T Cell Suppression.
[So] Source:J Immunol;193(12):5786-90, 2014 Dec 15.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:TLR play essential roles in the initiation and modulation of immune responses. TLR1/TLR2 heterodimers recognize triacylated bacterial lipopeptides, including the synthetic TLR1/2 lipopeptide Pam3CSK4. Genetic variation in TLR1 is associated with outcomes in diseases in which regulatory T cells (Treg) play a role, including asthma and allergy. To determine whether genetic polymorphisms in TLR1 are associated with alterations in Treg suppression of effector T cells (Teff), we performed in vitro suppression assays in healthy individuals with various haplotypes in TLR1. We show that functional genetic polymorphisms in TLR1 modify surface expression of TLR1 on T lymphocytes and confer enhanced Teff resistance to Treg suppression in the presence of Pam3CSK4. These effects are mediated, in part, by IL-6 and inhibited by blocking IL-6 signaling through STAT3. These findings suggest that TLR1 polymorphisms could influence immune-related disease through Teff resistance to Treg suppression.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1401185

  5 / 445370 MEDLINE  
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[PMID]: 25437445
[Au] Autor:Ito T; Sendai Y; Yamazaki S; Seki-Soma M; Hirose K; Watanabe M; Fukawa K; Nakauchi H
[Ad] Address:Pig Breeding Laboratory, Central Research Institute for Feed and Livestock, ZEN-NOH (National Federation of Agricultural Co-operative Associations), Hokkaido, Japan....
[Ti] Title:Generation of recombination activating gene-1-deficient neonatal piglets: a model of T and B cell deficient severe combined immune deficiency.
[So] Source:PLoS One;9(12):e113833, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Although severe combined immune deficiency (SCID) is a very important research model for mice and SCID mice are widely used, there are only few reports describing the SCID pig models. Therefore, additional research in this area is needed. In this study, we describe the generation of Recombination activating gene-1 (Rag-1)-deficient neonatal piglets in Duroc breed using somatic cell nuclear transfer (SCNT) with gene targeting and analysis using fluorescence-activated cell sorting (FACS) and histology. We constructed porcine Rag-1 gene targeting vectors for the Exon 2 region and obtained heterozygous/homozygous Rag-1 knockout cell colonies using SCNT. We generated two Rag-1-deficient neonatal piglets and compared them with wild-type neonatal piglets. FACS analysis showed that Rag-1 disruption causes a lack of Immunoglobulin M-positive B cells and CD3-positive T cells in peripheral blood mononuclear cells. Consistent with FACS analysis, histological analysis revealed structural defects and an absence of mature lymphocytes in the spleen, mesenteric lymph node (MLNs), and thymus in Rag-1-deficient piglets. These results confirm that Rag-1 is necessary for the generation of lymphocytes in pigs, and Rag-1-deficient piglets exhibit a T and B cell deficient SCID (T-B-SCID) phenotype similar to that of rodents and humans. The T-B-SCID pigs with Rag-1 deficiency generated in this study could be a suitably versatile model for laboratory, translational, and biomedical research, including the development of a humanized model and assessment of pluripotent stem cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0113833

  6 / 445370 MEDLINE  
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[PMID]: 25436994
[Au] Autor:Sharir R; Semo J; Shimoni S; Ben-Mordechai T; Landa-Rouben N; Maysel-Auslender S; Shaish A; Entin-Meer M; Keren G; George J
[Ad] Address:Heart Center, Kaplan Medical Center, Rehovot, Israel, Affiliated to the Hebrew University, Jerusalem, Israel; Laboratory of Cardiovascular Research, Department of Cardiology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel....
[Ti] Title:Experimental myocardial infarction induces altered regulatory T cell hemostasis, and adoptive transfer attenuates subsequent remodeling.
[So] Source:PLoS One;9(12):e113653, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Ischemic cardiac damage is associated with upregulation of cardiac pro-inflammatory cytokines, as well as invasion of lymphocytes into the heart. Regulatory T cells (Tregs) are known to exert a suppressive effect on several immune cell types. We sought to determine whether the Treg pool is influenced by myocardial damage and whether Tregs transfer and deletion affect cardiac remodeling. METHODS AND RESULTS: The number and functional suppressive activity of Tregs were assayed in mice subjected to experimental myocardial infarction. The numbers of splenocyte-derived Tregs in the ischemic mice were significantly higher after the injury than in the controls, and their suppressive properties were significantly compromised. Compared with PBS, adoptive Treg transfer to mice with experimental infarction reduced infarct size and improved LV remodeling and functional performance by echocardiography. Treg deletion with blocking anti-CD25 antibodies did not influence infarct size or echocardiographic features of cardiac remodeling. CONCLUSION: Treg numbers are increased whereas their function is compromised in mice with that underwent experimental infarction. Transfer of exogeneous Tregs results in attenuation of myocardial remodeling whereas their ablation has no effect. Thus, Tregs may serve as interesting potential interventional targets for attenuating left ventricular remodeling.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0113653

  7 / 445370 MEDLINE  
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[PMID]: 25320083
[Au] Autor:Hinz A; Jedamzick J; Herbring V; Fischbach H; Hartmann J; Parcej D; Koch J; Tampé R
[Ad] Address:From the Institute of Biochemistry, Biocenter and....
[Ti] Title:Assembly and Function of the Major Histocompatibility Complex (MHC) I Peptide-loading Complex Are Conserved Across Higher Vertebrates.
[So] Source:J Biol Chem;289(48):33109-17, 2014 Nov 28.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Antigen presentation to cytotoxic T lymphocytes via major histocompatibility complex class I (MHC I) molecules depends on the heterodimeric transporter associated with antigen processing (TAP). For efficient antigen supply to MHC I molecules in the ER, TAP assembles a macromolecular peptide-loading complex (PLC) by recruiting tapasin. In evolution, TAP appeared together with effector cells of adaptive immunity at the transition from jawless to jawed vertebrates and diversified further within the jawed vertebrates. Here, we compared TAP function and interaction with tapasin of a range of species within two classes of jawed vertebrates. We found that avian and mammalian TAP1 and TAP2 form heterodimeric complexes across taxa. Moreover, the extra N-terminal domain TMD0 of mammalian TAP1 and TAP2 as well as avian TAP2 recruits tapasin. Strikingly, however, only TAP1 and TAP2 from the same taxon can form a functional heterodimeric translocation complex. These data demonstrate that the dimerization interface between TAP1 and TAP2 and the tapasin docking sites for PLC assembly are conserved in evolution, whereas elements of antigen translocation diverged later in evolution and are thus taxon specific.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.M114.609263

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[PMID]: 25423176
[Au] Autor:Liu X; Xu Z; Zhu L; Liao S; Guo W
[Ad] Address:Animal Biotechnology Center, College of Veterinary Medicine, Sichuan Agricultural University, Ya' an, China....
[Ti] Title:Transcriptome Analysis of Porcine Thymus following Porcine Cytomegalovirus Infection.
[So] Source:PLoS One;9(11):e113921, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Porcine cytomegalovirus (PCMV) is a major immunosuppressive virus that mainly affects the immune function of T lymphocytes and macrophages. Despite being widely distributed around the world, no significantly different PCMV serotypes have been found. Moreover, the molecular immunosuppressive mechanisms of PCMV, along with the host antiviral mechanisms, are still not well characterized. To understand the potential impact of PCMV on the function of immune organs, we examined the transcriptome of PCMV-infected thymuses by microarray analysis. We identified 5,582 genes that were differentially expressed as a result of PCMV infection. Of these, 2,161 were upregulated and 3,421 were downregulated compared with the uninfected group. We confirmed the expression of 13 differentially expressed immune-related genes using quantitative real-time RT-PCR, and further confirmed the expression of six of those cytokines by western blot. Gene ontology, gene interaction networks, and KEGG pathway analysis of our results indicated that PCMV regulates multiple functional pathways, including the immune system, cellular and metabolic processes, networks of cytokine-cytokine receptor interactions, the TGF-ß signaling pathway, the lymphocyte receptor signaling pathway, and the TNF-α signaling pathway. Our study is the first comprehensive attempt to explore the host transcriptional response to PCMV infection in the porcine immune system. It provides new insights into the immunosuppressive molecular mechanisms and pathogenesis of PCMV. This previously unrecognized endogenous antiviral mechanism has implications for the development of host-directed strategies for the prevention and treatment of immunosuppressive viral diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0113921

  9 / 445370 MEDLINE  
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[PMID]: 25423108
[Au] Autor:de Carvalho JV; de Castro RO; da Silva EZ; Silveira PP; da Silva-Januário ME; Arruda E; Jamur MC; Oliver C; Aguiar RS; daSilva LL
[Ad] Address:Department of Cell and Molecular Biology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil....
[Ti] Title:Nef Neutralizes the Ability of Exosomes from CD4+ T Cells to Act as Decoys during HIV-1 Infection.
[So] Source:PLoS One;9(11):e113691, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Nef is an HIV-1 accessory protein that promotes viral replication and pathogenesis. A key function of Nef is to ensure sustained depletion of CD4 and MHC-I molecules in infected cells by inducing targeting of these proteins to multivesicular bodies (MVBs), and ultimately to lysosomes for degradation. Nef also affects cellular secretory routes promoting its own secretion via exosomes. To better understand the effects of Nef on the exocytic pathway, we investigated whether this viral factor modifies the composition of exosomes released by T lymphocytes. We showed that both CD4 and MHC-I molecules are secreted in exosomes from T cells and that the expression of Nef reduces the amount of these proteins in exosomes. To investigate the functional role for this novel activity of Nef, we performed in vitro HIV-1 infection assays in the presence of distinct populations of exosomes. We demonstrated that exosomes released by CD4+ T cells, but not CD4- T cells, efficiently inhibit HIV-1 infection in vitro. Because CD4 is the main receptor for HIV-1 infection, these results suggest that CD4 molecules displayed on the surface of exosomes can bind to envelope proteins of HIV-1 hindering virus interaction with target cells and infection. Importantly, CD4-depleted exosomes released by CD4+ T cells expressing Nef have a reduced capacity to inhibit HIV-1 infection in vitro. These results provide evidence that Nef promotes HIV-1 infection by reducing the expression of CD4 in exosomes from infected cells, besides the original role of Nef in reducing the CD4 levels at the cell surface.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0113691

  10 / 445370 MEDLINE  
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[PMID]: 25366203
[Au] Autor:Rathore AS; Kumar S; Konwar R; Makker A; Negi MP; Goel MM
[Ti] Title:CD3+, CD4+ & CD8+ tumour infiltrating lymphocytes (TILs) are predictors of favourable survival outcome in infiltrating ductal carcinoma of breast.
[So] Source:Indian J Med Res;140(3):361-9, 2014 Sep.
[Is] ISSN:0971-5916
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:BACKGROUND & OBJECTIVES: Tumour infiltrating lymphocytes (TILs) represent the host immune response against cancer cells associated with good or bad prognosis in different tumour types. This study was undertaken to evaluate the significance of CD3+, CD4+ and CD8+ TILs in breast cancer tissues in relation to clinico-pathological variables and survival outcome. METHODS: Immunohistochemistry (IHC) was performed with antibodies against CD3, CD4 and CD8 antigens on formalin-fixed paraffin-embedded tissue sections of 150 breast cancer patients. Intratumoural and stromal TIL counting was performed semiquantitatively. RESULTS: The higher CD3+, CD4+ and CD8+ intratumoural and stromal counts showed independent and direct association with good prognosis. The prognostic predictor value of intratumoural counts was higher than stromal counts. The independent associations of intratumoural and stromal counts became more prominent when adjusted with stage and grade, respectively. Among intratumoural counts, the high (++/+++) CD4+ count (OR=3.85, 95% CI=3.28-16.71, P<0.001) showed the highest survival followed by CD3+ (OR=2.70, 95% CI=1.76-8.30, P=0.001) and CD8+ (OR=2.58, 95% CI=1.55-5.86, p0 =0.001) the least when compared to respective low (+) counts. In contrast, among stromal counts, the high CD8+ count (OR=3.13, 95% CI=2.20-9.57, p0 <0.001) showed the highest survival followed by CD4+ (OR=3.02, 95% CI=2.07-8.89, p0 <0.001) and CD3+ (OR=2.45, 95% CI=1.53-6.73, p0 =0.002) the least. INTERPRETATION & CONCLUSIONS: Our results suggest that intratumoural CD4+ and stromal CD8+ counts by immunohistochemistry may serve as an independent prognosticator for favourable outcome in breast cancer.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review


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