Database : MEDLINE
Search on : Lymphocytes [Words]
References found : 453158 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 45316 go to page                         

  1 / 453158 MEDLINE  
              next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 26084511
[Au] Autor:MacParland SA; Chen AY; Corkum CP; Pham TN; Michalak TI
[Ad] Address:Molecular Virology and Hepatology Research Group, Division of BioMedical Sciences, Faculty of Medicine, Health Sciences Centre, Memorial University, St. John's, Newfoundland and Labrador, Canada. sonyamacparland@gmail.com....
[Ti] Title:Patient-derived hepatitis C virus inhibits CD4(+) but not CD8(+) T lymphocyte proliferation in primary T cells.
[So] Source:Virol J;12(1):93, 2015.
[Is] ISSN:1743-422X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Hepatitis C virus (HCV) can replicate in cells of the immune system and productively propagate in primary T lymphocytes in vitro. We aimed to determine whether exposure to authentic, patient-derived HCV can modify the proliferation capacity, susceptibility to apoptosis and phenotype of T cells. METHODS: Primary total T cells from a healthy donor were used as targets and plasma-derived HCV from patients with chronic hepatitis C served as inocula. T cell phenotype was determined prior to and at different time points after exposure to HCV. T cell proliferation and apoptosis were measured by flow cytometry-based assays. RESULTS: The HCV inocula that induced the highest intracellular expression of HCV also caused a greatest shift in the T cell phenotype from predominantly CD4-positive to CD8-positive. This shift was associated with inhibition of CD4+ but not CD8+ T cell proliferation and did not coincide with altered apoptotic death of either cell subset. CONCLUSIONS: The data obtained imply that exposure to native HCV can have an impact on the relative frequencies of CD4+ and CD8+ T cells by selectively suppressing CD4(+) T lymphocyte proliferation and this may occur in both the presence and the absence of measurable HCV replication in these cells. If the virus exerts a similar effect in vivo, it may contribute to the impairment of virus-specific T cell response by altering cooperation between immune cell subsets.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/s12985-015-0322-4

  2 / 453158 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 26084628
[Au] Autor:Ahmed M; Moremi N; Mirambo MM; Hokororo A; Mushi MF; Seni J; Kamugisha E; Mshana SE
[Ad] Address:Department of Pediatrics and Child Health, Weill Bugando School of Medicine, Catholic University of health and allied sciences, Mwanza, Tanzania. ahmedmaimuna@yahoo.co.uk....
[Ti] Title:Multi-resistant gram negative enteric bacteria causing urinary tract infection among malnourished underfives admitted at a tertiary hospital, northwestern, Tanzania.
[So] Source:Ital J Pediatr;41(1):44, 2015.
[Is] ISSN:1824-7288
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Infections are common complications occurring in malnourished childrenas a result of impaired immunity. Urinary tract infections (UTI) have been found to be the commonest cause of fever in normal children in developing countries. However, data regarding UTI among malnourished children is limited because in most of time severe and moderately malnourished children are afebrile despite significant bacteriuria. METHODS: A total of 402 malnourished underfives were enrolled. Demographic and other clinical characteristics were collected using standardized data collection tool. Urine specimens were cultured and interpreted according to standard operating procedures. Data were analyzed using STATA version 11. RESULTS: Out of 402 malnourished underfives, 229 (56.9 %) were male. The median age in months was 17 (IQR; 12-31). Of 402 malnourished underfives, 83 (20.3 %) had significant bacteriuria of gram negative enteric bacteria. Escherichia coli 35/84 and Klebsiella pneumonia 20/84 were predominant bacteria isolated. More than 37 % of isolates were resistant to third generation cephalosporins with all of them exhibiting extended spectrum beta lactamase (ESBL) phenotype. Rates of resistance to ampicillin, amoxillin/clavulanic acid, gentamicin and ciprofloxacin were 82/84 (98.7 %), 47/55 (85.4 %), 45/84 (57.8 %) and 9/84 (10.8 %) respectively. Decrease in age and increase in lymphocytes count were independent factors on multivariate logistic regression analysis found to predict UTI (p < 0.05). CONCLUSIONS: Multi-resistant gram negative enteric bacteria are common cause of UTI among underfives. A significant number of severe and moderate malnourished children with bacteriuria had no fever. Therefore, routine testing for UTI is emphasized in all malnourished underfives so that appropriate treatment can be initiated.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/s13052-015-0151-5

  3 / 453158 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26085210
[Au] Autor:Medvedev AE; Murphy M; Zhou H; Li X
[Ad] Address:Department of Immunology, University of Connecticut Health Center, Farmington, CT, USA....
[Ti] Title:E3 ubiquitin ligases Pellinos as regulators of pattern recognition receptor signaling and immune responses.
[So] Source:Immunol Rev;266(1):109-22, 2015 Jul.
[Is] ISSN:1600-065X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Pellinos are a family of E3 ubiquitin ligases discovered for their role in catalyzing K63-linked polyubiquitination of Pelle, an interleukin-1 (IL-1) receptor-associated kinase homolog in the Drosophila Toll pathway. Subsequent studies have revealed the central and non-redundant roles of mammalian Pellino-1, Pellino-2, and Pelino-3 in signaling pathways emanating from IL-1 receptors, Toll-like receptors, NOD-like receptors, T- and B-cell receptors. While Pellinos ability to interact with many signaling intermediates suggested their scaffolding roles, recent findings in mice expressing ligase-inactive Pellinos demonstrated the importance of Pellino ubiquitin ligase activity. Cell-specific functions of Pellinos have emerged, e.g. Pellino-1 being a negative regulator in T lymphocytes and a positive regulator in myeloid cells, and details of molecular regulation of receptor signaling by various members of the Pellino family have been revealed. In this review, we summarize current information about Pellino-mediated regulation of signaling by pattern recognition receptors, T-cell and B-cell receptors and tumor necrosis factor receptors, and discuss Pellinos roles in sepsis and infectious diseases, as well as in autoimmune, inflammatory, and allergic disorders. We also provide our perspective on the potential of targeting Pellinos with peptide- or small molecule-based drug compounds as a new therapeutic approach for septic shock and autoimmune pathologies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/imr.12298

  4 / 453158 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26085206
[Au] Autor:Lin WW; Hostager BS; Bishop GA
[Ad] Address:The Graduate Program in Immunology, University of Iowa, Iowa City, IA, USA....
[Ti] Title:TRAF3, ubiquitination, and B-lymphocyte regulation.
[So] Source:Immunol Rev;266(1):46-55, 2015 Jul.
[Is] ISSN:1600-065X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The signaling adapter protein tumor necrosis factor receptor (TNFR)-associated factor 3 (TRAF3) is both modified by and contributes to several types of ubiquitination events. TRAF3 plays a variety of context-dependent regulatory roles in all types of immune cells. In B lymphocytes, TRAF3 contributes to regulation of signaling by members of both the TNFR superfamily and innate immune receptors. TRAF3 also plays a unique cell type-specific and critical role in the restraint of B-cell homeostatic survival, a role with important implications for both B-cell differentiation and the pathogenesis of B-cell malignancies. This review focuses upon the relationship between ubiquitin and TRAF3, and how this contributes to multiple functions of TRAF3 in the regulation of signal transduction, transcriptional activation, and effector functions of B lymphocytes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/imr.12299

  5 / 453158 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text

[PMID]: 26085940
[Au] Autor:Matveeva OV; Kochneva GV; Netesov SV; Onikienko SB; Chumakov PM
[Ad] Address:Biopolymer Design, 23 Nylander Way, Acton, Massachusetts, United States....
[Ti] Title:Mechanisms of Oncolysis by Paramyxovirus Sendai.
[So] Source:Acta Naturae;7(2):6-16, 2015 Apr-Jun.
[Is] ISSN:2075-8251
[Cp] Country of publication:Russia (Federation)
[La] Language:eng
[Ab] Abstract:Some viral strains of the Paramyxoviridae family may be used as anti-tumor agents. Oncolytic paramyxoviruses include attenuated strains of the measles virus, Newcastle disease virus, and Sendai virus. These viral strains, and the Sendai virus in particular, can preferentially induce the death of malignant, rather than normal, cells. The death of cancer cells results from both direct killing by the virus and through virus-induced activation of anticancer immunity. Sialic-acid-containing glycoproteins that are overexpressed in cancer cells serve as receptors for some oncolytic paramyxoviruses and ensure preferential interaction of paramyxoviruses with malignant cells. Frequent genetic defects in interferon and apoptotic response systems that are common to cancer cells ensure better susceptibility of malignant cells to viruses. The Sendai virus as a Paramyxovirus is capable of inducing the formation of syncytia, multinuclear cell structures which promote viral infection spread within a tumor without virus exposure to host neutralizing antibodies. As a result, the Sendai virus can cause mass killing of malignant cells and tumor destruction. Oncolytic paramyxoviruses can also promote the immune-mediated elimination of malignant cells. In particular, they are powerful inducers of interferon and other cytokynes promoting antitumor activity of various cell components of the immune response, such as dendritic and natural killer cells, as well as cytotoxic T lymphocytes. Taken together these mechanisms explain the impressive oncolytic activity of paramyxoviruses that hold promise as future, efficient anticancer therapeutics.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Da] Date of entry for processing:150618
[St] Status:PubMed-not-MEDLINE

  6 / 453158 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 25864722
[Au] Autor:Chang SC; Huq R; Chhabra S; Beeton C; Pennington MW; Smith BJ; Norton RS
[Ad] Address:Medicinal Chemistry, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Vic., Australia....
[Ti] Title:N-terminally extended analogues of the K(+) channel toxin from Stichodactyla helianthus as potent and selective blockers of the voltage-gated potassium channel Kv1.3.
[So] Source:FEBS J;282(12):2247-59, 2015 Jun.
[Is] ISSN:1742-4658
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The voltage-gated potassium channel Kv1.3 is an important target for the treatment of autoimmune diseases and asthma. Blockade of Kv1.3 by the sea anemone peptide K(+) -channel toxin from Stichodactyla helianthus (ShK) inhibits the proliferation of effector memory T lymphocytes and ameliorates autoimmune diseases in animal models. However, the lack of selectivity of ShK for Kv1.3 over the Kv1.1 subtype has driven a search for Kv1.3-selective analogues. In the present study, we describe N-terminally extended analogues of ShK that contain a negatively-charged Glu, designed to mimic the phosphonate adduct in earlier Kv1.3-selective analogues, and consist entirely of common protein amino acids. Molecular dynamics simulations indicated that a Trp residue at position [-3] of the tetrapeptide extension could form stable interactions with Pro377 of Kv1.3 and best discriminates between Kv1.3 and Kv1.1. This led to the development of ShK with an N-terminal Glu-Trp-Ser-Ser extension ([EWSS]ShK), which inhibits Kv1.3 with an IC50 of 34 pm and is 158-fold selective for Kv1.3 over Kv1.1. In addition, [EWSS]ShK is more than 2900-fold more selective for Kv1.3 over Kv1.2 and KCa3.1 channels. As a highly Kv1.3-selective analogue of ShK based entirely on protein amino acids, which can be produced by recombinant expression, this peptide is a valuable addition to the complement of therapeutic candidates for the treatment of autoimmune diseases.
[Pt] Publication type:EDITORIAL
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/febs.13294

  7 / 453158 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 25850866
[Au] Autor:Shibata AR; Troster EJ; Wong HR
[Ad] Address:1Pediatric Intensive Care Unit, Department of Pediatrics, Hospital Israelita Albert Einstein, Sao Paulo, Brazil. 2Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center and Cincinnati Children's Hospital Research Foundation, Cincinnati, OH.
[Ti] Title:Glucocorticoid Receptor Expression in Peripheral WBCs of Critically Ill Children.
[So] Source:Pediatr Crit Care Med;16(5):e132-40, 2015 Jun.
[Is] ISSN:1529-7535
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVES: To characterize glucocorticoid receptor expression in peripheral WBCs of critically ill children using flow cytometry. DESIGN: Prospective observational cohort. SETTING: A university-affiliated, tertiary PICU. PATIENTS: Fifty-two critically ill children. INTERVENTIONS: Samples collected for measurement of glucocorticoid receptor expression and parallel cortisol levels. MEASUREMENTS AND MAIN RESULTS: Subjects with cardiovascular failure had significantly lower glucocorticoid receptor expression both in CD4 lymphocytes (mean fluorescence intensity, 522 [354-787] vs 830 [511-1,219]; p = 0.036) and CD8 lymphocytes (mean fluorescence intensity, 686 [350-835] vs 946 [558-1,511]; p = 0.019) compared with subjects without cardiovascular failure. Subjects in the upper 50th percentile of Pediatric Risk of Mortality III scores and organ failure also had significantly lower glucocorticoid receptor expression in CD4 and CD8 lymphocytes. There was no linear correlation between cortisol concentrations and glucocorticoid receptor expression. CONCLUSIONS: Our study suggests that patients with shock and increased severity of illness have lower glucocorticoid receptor expression in CD4 and CD8 lymphocytes. Glucocorticoid receptor expression does not correlate well with cortisol levels. Future studies could focus on studying glucocorticoid receptor expression variability and isoform distribution in the pediatric critically ill population as well as on different strategies to optimize glucocorticoid response.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/PCC.0000000000000407

  8 / 453158 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 25903330
[Au] Autor:Schafer JL; Li H; Evans TI; Estes JD; Reeves RK
[Ad] Address:Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA....
[Ti] Title:Accumulation of Cytotoxic CD16+ NK Cells in Simian Immunodeficiency Virus-Infected Lymph Nodes Associated with In Situ Differentiation and Functional Anergy.
[So] Source:J Virol;89(13):6887-94, 2015 Jul 1.
[Is] ISSN:1098-5514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:UNLABELLED: Recent evidence suggests that even in treated infections, human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) replication may continue in lymph nodes (LN), serving as a potential virus reservoir. Here we investigated the effects of lentivirus infection on natural killer (NK) cell frequencies, phenotypes, and functions in naive and acutely or chronically SIVmac239-infected rhesus macaques. Compared to that in naive animals, we observed a 3-fold-greater frequency of cytotoxic CD16(+) CD56(-) NK cells in LN of chronically infected macaques. However, NK cells did not appear to be trafficking to LN, as homing markers CD62L and CCR7 did not increase on circulating NK cells during infection. LN NK cells demonstrated enhanced cytotoxicity in acute infection, with 2-fold increases in perforin expression and 3-fold increases in CD107a expression following mitogen stimulation. Lysis of K562 cells by LN NK cells from acutely infected animals was greater than lysis by preinfection samples from the same animals. LN NK cells from chronically infected animals lysed K562 cells more efficiently than LN NK cells from uninfected animals, but importantly, surrogate markers of cytotoxicity in infected macaques were disproportionately greater than ex vivo killing. Furthermore, Tim-3, an indicator of activation and/or exhaustion, was upregulated 3-fold on LN NK cells in chronically infected animals. Collectively, these data suggest that LN NK cells are skewed toward a cytotoxic phenotype during SIV infection but may become dysfunctional and exhausted in chronic disease. IMPORTANCE: The accumulation of CD16(+) CD56(-) NK cells in the SIV-infected lymph node without changes in NK homing to the LN could suggest that these cells are differentiating in situ. Surprisingly, this increase in frequency of the cytotoxic subset of NK cells is not accompanied by an increase of similar magnitude in the cytolytic function of LN lymphocytes. This functional modulation, together with the higher Tim-3 expression observed on LN NK cells isolated from chronically infected animals than on those from naive macaques, is indicative of an exhausted phenotype. This exhaustion could contribute to the robust replication of HIV and SIV in the LN during acute and chronic stages of infection, allowing the survival of infected cells and maintenance of a viral reservoir.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1128/JVI.00660-15

  9 / 453158 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 25849247
[Au] Autor:Narni-Mancinelli E; Vivier E
[Ad] Address:1] Centre d'Immunologie de Marseille-Luminy, UM2 Aix-Marseille Université, Marseille, France [2] INSERM U1104, Marseille, France [3] CNRS UMR7280, Marseille, France.
[Ti] Title:Shed NKG2D ligand boosts NK cell immunity.
[So] Source:Cell Res;25(6):651-2, 2015 Jun.
[Is] ISSN:1748-7838
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Ligands for natural killer (NK) cell activating receptors can be released from tumor cells and are believed to promote tumor growth by acting as decoys for effector lymphocytes. In a recent paper published in Science, Deng et al. report another scenario in which a shed form of the MULT1 mouse NKG2D ligand boosts NK cell functions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/cr.2015.41

  10 / 453158 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 25791085
[Au] Autor:Yang S; Fujikado N; Kolodin D; Benoist C; Mathis D
[Ad] Address:Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA. Aging Intervention Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, Yuseong-gu, Daejeon, 305-806, South Korea....
[Ti] Title:Immune tolerance. Regulatory T cells generated early in life play a distinct role in maintaining self-tolerance.
[So] Source:Science;348(6234):589-94, 2015 May 1.
[Is] ISSN:1095-9203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aire is an important regulator of immunological tolerance, operating in a minute subset of thymic stromal cells to induce transcripts encoding peptides that guide T cell selection. Expression of Aire during a perinatal age window is necessary and sufficient to prevent the multiorgan autoimmunity characteristic of Aire-deficient mice. We report that Aire promotes the perinatal generation of a distinct compartment of Foxp3(+)CD4(+) regulatory T (Treg) cells, which stably persists in adult mice. This population has a role in maintaining self-tolerance, a transcriptome and an activation profile distinguishable from those of Tregs produced in adults. Underlying the distinct Treg populations are age-dependent, Aire-independent differences in the processing and presentation of thymic stromal-cell peptides, resulting in different T cell receptor repertoires. Our findings expand the notion of a developmentally layered immune system.
[Mh] MeSH terms primary: Self Tolerance/genetics
T-Lymphocytes, Regulatory/immunology
Transcription Factors/physiology
[Mh] MeSH terms secundary: Animals
Antigens, CD4/analysis
Autoimmunity
Forkhead Transcription Factors/analysis
Mice
Mice, Knockout
Receptors, Antigen, T-Cell/immunology
Transcription Factors/genetics
Transcriptome
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (APECED protein); 0 (Antigens, CD4); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Receptors, Antigen, T-Cell); 0 (Transcription Factors)
[Em] Entry month:1505
[Cu] Class update date: 150621
[Lr] Last revision date:150621
[Js] Journal subset:IM
[Da] Date of entry for processing:150501
[St] Status:MEDLINE
[do] DOI:10.1126/science.aaa7017


page 1 of 45316 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information