Database : MEDLINE
Search on : Lymphocytes [Words]
References found : 465706 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 46571 go to page                         

  1 / 465706 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 26946113
[Au] Autor:Li H; Wang Y; Han Z; Wang Y; Liang S; Jiang L; Hu Y; Kong X; Liu S
[Ad] Address:Division of Avian Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150001, PR China....
[Ti] Title:Recombinant duck enteritis viruses expressing major structural proteins of the infectious bronchitis virus provide protection against infectious bronchitis in chickens.
[So] Source:Antiviral Res;130:19-26, 2016 Jun.
[Is] ISSN:1872-9096
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:To design an alternative vaccine for control of infectious bronchitis in chickens, three recombinant duck enteritis viruses (rDEVs) expressing the N, S, or S1 protein of infectious bronchitis virus (IBV) were constructed using conventional homologous recombination methods, and were designated as rDEV-N, rDEV-S, and rDEV-S1, respectively. Chickens were divided into five vaccinated groups, which were each immunized with one of the rDEVs, covalent vaccination with rDEV-N & rDEV-S, or covalent vaccination with rDEV-N & rDEV-S1, and a control group. An antibody response against IBV was detectable and the ratio of CD4(+)/CD8(+) T-lymphocytes decreased at 7 days post-vaccination in each vaccinated group, suggesting that humoral and cellular responses were elicited in each group as early as 7 days post-immunization. After challenge with a homologous virulent IBV strain at 21 days post-immunization, vaccinated groups showed significant differences in the percentage of birds with clinical signs, as compared to the control group (p<0.01), as the two covalent-vaccination groups and the rDEV-S group provided better protection than the rDEV-N- or rDEV-S1-vaccinated group. There was less viral shedding in the rDEV-N & rDEV-S- (2/10) and rDEV-N & rDEV-S1- (2/10) vaccinated groups than the other three vaccinated groups. Based on the clinical signs, viral shedding, and mortality rates, rDEV-N & rDEV-S1 covalent vaccination conferred better protection than use of any of the single rDEVs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1605
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 465706 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26578649
[Au] Autor:Ligocki AJ; Brown JR; Niederkorn JY
[Ad] Address:Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas, USA jerry.niederkorn@utsouthwestern.edu.
[Ti] Title:Role of interferon-γ and cytotoxic T lymphocytes in intraocular tumor rejection.
[So] Source:J Leukoc Biol;99(5):735-47, 2016 May.
[Is] ISSN:1938-3673
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The eye is normally an immunosuppressive environment. This condition is better known as immune privilege and protects the eye from immune-mediated inflammation of tissues that cannot regenerate. However, immune privilege creates a dilemma for the eye when intraocular neoplasms arise. In some cases, immune privilege is suspended, resulting in the immune rejection of intraocular tumors. This study employed a mouse model in which interferon-γ-dependent intraocular tumor rejection occurs. We tested the hypothesis that this rejection requires interferon-γ for the generation and functional capacity of cytotoxic T lymphocyte-mediated rejection of intraocular tumors. Tumors grew progressively in the eyes of interferon-γ knockout mice, even though the mice generated tumor-specific cytotoxic T lymphocyte responses in the periphery. However, interferon-γ knockout mice rejected tumors that were introduced into extraocular sites. Subcutaneous tumor immunization before intraocular challenge led to tumor rejection and preservation of the eye in wild-type mice. By contrast, tumors grew progressively in the eyes of interferon-γ knockout mice despite their ability to generate peripheral tumor-specific cytotoxic T lymphocytes as well as the capacity of CD8(+) T cells to enter the eye as shown by the presence of CD8 and perforin message and CD3(+)CD8(+) leukocytes within the tumor-bearing eye. We found that cytotoxic T lymphocytes generated in wild-type mice and adoptively transferred into interferon-γ knockout mice mediated the rejection of intraocular tumors in interferon-γ knockout hosts. The results indicate that interferon-γ is critical for the initial priming and differentiation of cytotoxic T lymphocytes residing in the periphery to produce the most effect antitumor function within the eye.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160430
[Lr] Last revision date:160430
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1189/jlb.3A0315-093RRR

  3 / 465706 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26884334
[Au] Autor:Jattani RP; Tritapoe JM; Pomerantz JL
[Ad] Address:From the Department of Biological Chemistry, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
[Ti] Title:Intramolecular Interactions and Regulation of Cofactor Binding by the Four Repressive Elements in the Caspase Recruitment Domain-containing Protein 11 (CARD11) Inhibitory Domain.
[So] Source:J Biol Chem;291(16):8338-48, 2016 Apr 15.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The CARD11 signaling scaffold transmits signaling between antigen receptors on B and T lymphocytes and the transcription factor NF-κB during the adaptive immune response. CARD11 activity is controlled by an inhibitory domain (ID), which participates in intramolecular interactions and prevents cofactor binding prior to receptor triggering. Oncogenic CARD11 mutations associated with the activated B cell-like subtype of diffuse large B cell lymphoma somehow perturb ID-mediated autoinhibition to confer CARD11 with the dysregulated spontaneous signaling to NF-κB that is required for the proliferation and survival of the lymphoma. Here, we investigate how the four repressive elements (REs) we have discovered in the CARD11 ID function to inhibit CARD11 activity with cooperativity and redundancy. We find that each RE contributes to the maintenance of the closed inactive state of CARD11 that predominates in the absence of receptor engagement. Each RE also contributes to the prevention of Bcl10 binding in the basal unstimulated state. RE1, RE2, and RE3 participate in intramolecular interactions with other CARD11 domains and share domain targets for binding. Remarkably, diffuse large B cell lymphoma-associated gain-of-function mutations in the caspase recruitment domain, LATCH, or coiled coil can perturb intramolecular interactions mediated by multiple REs, suggesting how single amino acid oncogenic CARD11 mutations can perturb or bypass the action of redundant inhibitory REs to achieve the level of hyperactive CARD11 signaling required to support lymphoma growth.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160430
[Lr] Last revision date:160430
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.M116.717322

  4 / 465706 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26826124
[Au] Autor:Liu X; Berry CT; Ruthel G; Madara JJ; MacGillivray K; Gray CM; Madge LA; McCorkell KA; Beiting DP; Hershberg U; May MJ; Freedman BD
[Ad] Address:From the Departments of Pathobiology and....
[Ti] Title:T Cell Receptor-induced Nuclear Factor κB (NF-κB) Signaling and Transcriptional Activation Are Regulated by STIM1- and Orai1-mediated Calcium Entry.
[So] Source:J Biol Chem;291(16):8440-52, 2016 Apr 15.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:T cell activation following antigen binding to the T cell receptor (TCR) involves the mobilization of intracellular Ca(2+) to activate the key transcription factors nuclear factor of activated T lymphocytes (NFAT) and NF-κB. The mechanism of NFAT activation by Ca(2+) has been determined. However, the role of Ca(2+) in controlling NF-κB signaling is poorly understood, and the source of Ca(2+) required for NF-κB activation is unknown. We demonstrate that TCR- but not TNF-induced NF-κB signaling upstream of IκB kinase activation absolutely requires the influx of extracellular Ca(2+) via STIM1-dependent Ca(2+) release-activated Ca(2+)/Orai channels. We further show that Ca(2+) influx controls phosphorylation of the NF-κB protein p65 on Ser-536 and that this posttranslational modification controls its nuclear localization and transcriptional activation. Notably, our data reveal that this role for Ca(2+) is entirely separate from its upstream control of IκBα degradation, thereby identifying a novel Ca(2+)-dependent distal step in TCR-induced NF-κB activation. Finally, we demonstrate that this control of distal signaling occurs via Ca(2+)-dependent PKCα-mediated phosphorylation of p65. Thus, we establish the source of Ca(2+) required for TCR-induced NF-κB activation and define a new distal Ca(2+)-dependent checkpoint in TCR-induced NF-κB signaling that has broad implications for the control of immune cell development and T cell functional specificity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160430
[Lr] Last revision date:160430
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.M115.713008

  5 / 465706 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26550921
[Au] Autor:Bai Y; Krishnamoorthy N; Patel KR; Rosas I; Sanderson MJ; Ai X
[Ad] Address:1 Pulmonary, Allergy, Sleep and Critical Care Medicine, Boston University School of Medicine, Boston, Massachusetts....
[Ti] Title:Cryopreserved Human Precision-Cut Lung Slices as a Bioassay for Live Tissue Banking. A Viability Study of Bronchodilation with Bitter-Taste Receptor Agonists.
[So] Source:Am J Respir Cell Mol Biol;54(5):656-63, 2016 May.
[Is] ISSN:1535-4989
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Human precision-cut lung slices (hPCLSs) provide a unique ex vivo model for translational research. However, the limited and unpredictable availability of human lung tissue greatly impedes their use. Here, we demonstrate that cryopreservation of hPCLSs facilitates banking of live human lung tissue for routine use. Our results show that cryopreservation had little effect on overall cell viability and vital functions of immune cells, including phagocytes and T lymphocytes. In addition, airway contraction and relaxation in response to specific agonists and antagonists, respectively, were unchanged after cryopreservation. At the subcellular level, cryopreserved hPCLSs maintained Ca(2+)-dependent regulatory mechanisms for the control of airway smooth muscle cell contractility. To exemplify the use of cryopreserved hPCLSs in smooth muscle research, we provide evidence that bitter-taste receptor (TAS2R) agonists relax airways by blocking Ca(2+) oscillations in airway smooth muscle cells. In conclusion, the banking of cryopreserved hPCLSs provides a robust bioassay for translational research of lung physiology and disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160430
[Lr] Last revision date:160430
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1165/rcmb.2015-0290MA

  6 / 465706 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 27123161
[Au] Autor:Han SC; Kang NJ; Yoon WJ; Kim S; Na MC; Koh YS; Hyun JW; Lee NH; Ko MH; Kang HK; Yoo ES
[Ad] Address:Department of Medicine, School of Medicine, Jeju National University, Jeju, Korea....
[Ti] Title:External Application of Apo-9'-fucoxanthinone, Isolated from Sargassum muticum, Suppresses Inflammatory Responses in a Mouse Model of Atopic Dermatitis.
[So] Source:Toxicol Res;32(2):109-14, 2016 Apr.
[Is] ISSN:1976-8257
[Cp] Country of publication:Korea (South)
[La] Language:eng
[Ab] Abstract:Allergic skin inflammation such as atopic dermatitis is characterized by skin barrier dysfunction, edema, and infiltration with various inflammatory cells. The anti-inflammatory effects of Apo-9'-fucoxanthinone, isolated from Sargassum muticum, have been described in many diseases, but the mechanism by which it modulates the immune system is poorly understood. In this study, the ability of Apo-9'-fucoxanthinone to suppress allergic reactions was investigated using a mouse model of atopic dermatitis. The Apo-9'-fucoxanthinone-treated group showed significantly decreased immunoglobulin E in serum. Also, Apo-9'-fucoxanthinone treatment resulted in a smaller lymph node size with reduced the thickness and length compared to the induction group. In addition, Apo-9'-fucoxanthinone inhibited the expression of interleukin-4, interferon-gamma and tumor necrosis factor-alpha by phorbol 12-myristate 13-acetate and ionomycin-stimulated lymphocytes. These results suggest that Apo-9'-fucoxanthinone may be a useful therapeutic strategy for treating chronic inflammatory diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160430
[Lr] Last revision date:160430
[Da] Date of entry for processing:160428
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.5487/TR.2016.32.2.109

  7 / 465706 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 27123464
[Au] Autor:Barton JC; Bertoli LF; Barton JC; Acton RT
[Ad] Address:Department of Medicine, Brookwood Medical Center, Birmingham, AL 35209, USA; Southern Iron Disorders Center, Birmingham, AL 35209, USA; Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35209, USA....
[Ti] Title:Selective Subnormal IgG1 in 54 Adult Index Patients with Frequent or Severe Bacterial Respiratory Tract Infections.
[So] Source:J Immunol Res;2016:1405950, 2016.
[Is] ISSN:2314-7156
[Cp] Country of publication:Egypt
[La] Language:eng
[Ab] Abstract:We characterized 54 adult index patients with reports of frequent or severe bacterial respiratory tract infections at diagnosis of selective subnormal IgG1. Mean age was 50 13 (SD) y; 87.0% were women. Associated disorders included the following: autoimmune conditions 50.0%; hypothyroidism 24.1%; atopy 38.9%; and other allergy 31.5%. In 35.5%, proportions of protective S. pneumoniae serotype-specific IgG levels did not increase after polyvalent pneumococcal polysaccharide vaccination (PPPV). Blood lymphocyte subset levels were within reference limits in most patients. Regressions on IgG1 and IgG3 revealed no significant association with age, sex, autoimmune conditions, hypothyroidism, atopy, other allergy, corticosteroid therapy, or lymphocyte subsets. Regression on IgG2 revealed significant associations with PPPV response (negative) and CD19+ lymphocytes (positive). Regression on IgG4 revealed significant positive associations with episodic corticosteroid use and IgA. Regression on IgA revealed positive associations with IgG2 and IgG4. Regression on IgM revealed negative associations with CD56+/CD16+ lymphocytes. Regressions on categories of infection revealed a negative association of urinary tract infections and IgG1. HLA-A(⁎)03, HLA-B(⁎)55 and HLA-A(⁎)24, HLA-B(⁎)35 haplotype frequencies were greater in 38 patients than 751 controls. We conclude that nonprotective S. pneumoniae IgG levels and atopy contribute to increased susceptibility to respiratory tract infections in patients with selective subnormal IgG1.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160430
[Lr] Last revision date:160430
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1155/2016/1405950

  8 / 465706 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 27064903
[Au] Autor:Verbist KC; Guy CS; Milasta S; Liedmann S; Kaminski MM; Wang R; Green DR
[Ad] Address:Department of Immunology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, Tennessee 38105, USA....
[Ti] Title:Metabolic maintenance of cell asymmetry following division in activated T lymphocytes.
[So] Source:Nature;532(7599):389-93, 2016 Apr 21.
[Is] ISSN:1476-4687
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Asymmetric cell division, the partitioning of cellular components in response to polarizing cues during mitosis, has roles in differentiation and development. It is important for the self-renewal of fertilized zygotes in Caenorhabditis elegans and neuroblasts in Drosophila, and in the development of mammalian nervous and digestive systems. T lymphocytes, upon activation by antigen-presenting cells (APCs), can undergo asymmetric cell division, wherein the daughter cell proximal to the APC is more likely to differentiate into an effector-like T cell and the distal daughter is more likely to differentiate into a memory-like T cell. Upon activation and before cell division, expression of the transcription factor c-Myc drives metabolic reprogramming, necessary for the subsequent proliferative burst. Here we find that during the first division of an activated T cell in mice, c-Myc can sort asymmetrically. Asymmetric distribution of amino acid transporters, amino acid content, and activity of mammalian target of rapamycin complex 1 (mTORC1) is correlated with c-Myc expression, and both amino acids and mTORC1 activity sustain the differences in c-Myc expression in one daughter cell compared to the other. Asymmetric c-Myc levels in daughter T cells affect proliferation, metabolism, and differentiation, and these effects are altered by experimental manipulation of mTORC1 activity or c-Myc expression. Therefore, metabolic signalling pathways cooperate with transcription programs to maintain differential cell fates following asymmetric T-cell division.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1604
[Cu] Class update date: 160430
[Lr] Last revision date:160430
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/nature17442

  9 / 465706 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 27104612
[Au] Autor:Ameratunga M; Asadi K; Lin X; Walkiewicz M; Murone C; Knight S; Mitchell P; Boutros P; John T
[Ad] Address:Department of Medical Oncology, Austin Health, Olivia-Newton John Cancer and Wellness Centre, Victoria, Australia....
[Ti] Title:PD-L1 and Tumor Infiltrating Lymphocytes as Prognostic Markers in Resected NSCLC.
[So] Source:PLoS One;11(4):e0153954, 2016.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Immune checkpoint inhibition has shifted treatment paradigms in non-small cell lung cancer (NSCLC). Conflicting results have been reported regarding the immune infiltrate and programmed death-ligand 1 (PD-L1) as a prognostic marker. We correlated the immune infiltrate and PD-L1 expression with clinicopathologic characteristics in a cohort of resected NSCLC. METHODS: A tissue microarray was constructed using triplicate cores from consecutive resected NSCLC. Immunohistochemistry was performed for CD8, FOXP3 and PD-L1. Strong PD-L1 expression was predefined as greater than 50% tumor cell positivity. Matched nodal samples were assessed for concordance of PD-L1 expression. RESULTS: Of 522 patients, 346 were node-negative (N0), 72 N1 and 109 N2; 265 were adenocarcinomas (AC), 182 squamous cell cancers (SCC) and 75 other. Strong PD-L1 expression was found in 24% cases. In the overall cohort, PD-L1 expression was not associated with survival. In patients with N2 disease, strong PD-L1 expression was associated with significantly improved disease-free (DFS) and overall survival (OS) in multivariate analysis (HR 0.49, 95%CI 0.36-0.94, p = 0.031; HR 0.46, 95%CI 0.26-0.80, p = 0.006). In this resected cohort only 5% harboured EGFR mutations, whereas 19% harboured KRAS and 23% other. KRAS mutated tumors were more likely to highly express PD-L1 compared to EGFR (22% vs 3%). A stromal CD8 infiltrate was associated with significantly improved DFS in SCC (HR 0.70, 95%CI 0.50-0.97, p = 0.034), but not AC, whereas FOXP3 was not prognostic. Matched nodal specimens (N = 53) were highly concordant for PD-L1 expression (89%). CONCLUSION: PD-L1 expression was not prognostic in the overall cohort. PD-L1 expression in primary tumor and matched nodal specimens were highly concordant. The observed survival benefit in N2 disease requires confirmation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160430
[Lr] Last revision date:160430
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0153954

  10 / 465706 MEDLINE  
              first record previous record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 27100663
[Au] Autor:Rizk HH; Hamdy NM; Al-Ansari NL; El-Mesallamy HO
[Ad] Address:Biochemistry Department, Faculty of Pharmacy, Ain-Shams University, Cairo, Egypt....
[Ti] Title:Pretreatment Predictors of Response to PegIFN-RBV Therapy in Egyptian Patients with HCV Genotype 4.
[So] Source:PLoS One;11(4):e0153895, 2016.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Egypt has the highest prevalence of a difficult to treat chronic hepatitis C virus (HCV), genotype 4. Pretreatment factors could guide individualization of therapy which aids in treatment optimization and interleukin IL28B gene polymorphism has been shown to closely relate to HCV treatment response. Polymorphisms in genes encoding inhibitors of T-cell response, which have role in disease progression as Programmed Cell Death 1 (PD-1), and Cytotoxic T-Lymphocytes Antigen-4 (CTLA-4), could be candidate markers predicting treatment response. METHODS: This cohort study consisted of 200 chronic HCV genotype 4 infected patients treated with PegIFN α-2a and RBV in 2 hepatology centers. Genotyping of the polymorphisms in the IL28B gene region (rs12979860), PD1.3 (rs11568821) and CTLA-4 (rs231775) was performed on DNA collected from each patient using TaqMan genotyping assay. Groups were classified according to response into sustained virological responders (SVR), or non-responders (NR). A multivariate logistic regression analysis was used to identify potential markers, host pretreatment clinical and viral predictive factors including viral load, insulin resistance, and alpha fetoprotein (AFP) related to treatment response. RESULTS: Our results showed that in a multivariate analyses IL28B C/C genotype was the most significant predictor for SVR (OR = 10.86; p<0.0001) followed by AFP (OR = 0.915; p = 0.001) then CTLA-4/G genotypes (OR = 1.948; p = 0.022). However, PD-1.3/A genotypes and platelets count were significantly related to response in univariate analysis only (OR = 1.973; p = 0.023; OR = 1.007; p = 0.009 respectively). CONCLUSION: IL28B SNP, AFP level, and CTLA-4 SNP could be used in conjunction to predict treatment response in HCV genotype 4 infected Egyptian patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160430
[Lr] Last revision date:160430
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0153895


page 1 of 46571 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