Database : MEDLINE
Search on : Lymphocytes [Words]
References found : 461132 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 46114 go to page                         

  1 / 461132 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 26655144
[Au] Autor:Yang W; Yan H; Ma Y; Yu T; Guo H; Kuang Y; Ren R; Li J
[Ad] Address:Institute of Tropical Medicine, Third Military Medical University, Gaotanyan Street 30, Chongqing 400038, China....
[Ti] Title:Lower activation-induced T-cell apoptosis is related to the pathological immune response in secondary infection with hetero-serotype dengue virus.
[So] Source:Immunobiology;221(3):432-9, 2016 Mar.
[Is] ISSN:1878-3279
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The available evidence suggests that dengue virus-specific T lymphocytes and cytokine storm play a pivotal role in the immunopathogenesis of plasma leakage. Investigations are underway to identify the immune profiles associated with increased or decreased risk for severe disease. In this study, CD14+ cells from the peripheral blood mononuclear cells (PBMCs) of patients who recovered from DENV-1 infection were infected with DENV-1 or DENV-2 and co-cultured with memory T cells. We found that secondary infection with DENV-2 suppresses the cell reproductive capacity but forms more cell clones and more functional cells to produce more proinflammatory factors (IFN-γ, TNF-α, IL-6, IL-8, IL-12 and IL-17) and less regulatory cytokines (IL-10, TGF-ß) which results in higher viral replication compared to secondary infection with DENV-1. Memory dengue virus-specific T cells which are induced in a primary dengue virus infection are reactivated by the heterologous serotype of dengue virus and antigen-presenting cells (APCs) during a secondary infection. Dramatically, less apoptosis and more continuous activation of T cells in secondary infection with hetero-serotype DENV were observed. This discovery which has not been reported previously may be the reasonable and vital interpretation for the cytokine storm and severe symptoms observed in secondary infection with DENV. In summary, secondary infection with hetero-serotype DENV elicits the relatively pathological immune response while secondary infection with homologous-serotype DENV induces the relatively protective immune response by activation-induced cell death (AICD) of T cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 461132 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26652243
[Au] Autor:Costa RA; Matos LB; Cantaruti TA; de Souza KS; Vaz NM; Carvalho CR
[Ad] Address:Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Av. Antônio Carlos 6627, Pampulha, Belo Horizonte, MG CEP: 31270-901, Brazil....
[Ti] Title:Systemic effects of oral tolerance reduce the cutaneous scarring.
[So] Source:Immunobiology;221(3):475-85, 2016 Mar.
[Is] ISSN:1878-3279
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Immunological tolerance refer to the inhibition of specific immune responsiveness and the ingestion of proteins previous to immunization is a reliable method to induce (oral) tolerance. Parenteral exposure to tolerated antigens, in adjuvant, trigger indirect and systemic effects that inhibits concomitant immune responses to other unrelated antigens and also decrease unrelated inflammatory responses. Interesting, intraperitoneal (i.p.) exposure to orally-tolerated proteins soon before an incisional linear skin wound improves the healing by primary intention in mice. An important clinical and surgical objective is to identify strategies to improve wound healing and reduce scarring. OBJECTIVE: To evaluate whether i.p. injection of an orally-tolerated protein improves wound healing by secondary intention and reduce scarring of full-thickness excisional skin injury. METHODS: C57Bl/6 mice were turned tolerant to ovalbumin (OVA) by drinking a solution containing OVA; seven days later, they received an i.p. injection of OVA plus Al(OH)3 adjuvant immediately before two full-thickness excisional skin wounds, under anesthesia. The wound healing process was evaluated macro and microscopically after H&E, toluidine blue and Gomori's Trichrome staining. The presence of granulocytes, macrophages, miofibroblasts, fibronectin, collagen I and collagen III was investigated by immunofluorescence and the levels of cytokines by flow cytometry or ELISA. Mice not tolerant to OVA were included as controls. RESULTS: The i.p. injection of OVA+Al(OH)3 in mice orally tolerant to OVA reduced the subsequent inflammatory response in the wound bed and the cutaneous scarring. There was a change in the pattern of collagen deposition making it more similar to the pattern observed in intact skin. In tolerant mice, mast cells and granulocytes (Ly-6C/G+), were reduced, while lymphocytes (CD3+) were increased in the wound bed. Time course analysis of Th1/Th2/Th17 cytokines and growth factors showed slightly differences between tolerant and control groups. CONCLUSION: Parenteral injection of an orally-tolerated protein has systemic consequences that impair the inflammatory response triggered by skin injury and reduce the cutaneous scarring.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Js] Journal subset:IM
[St] Status:In-Data-Review

  3 / 461132 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26700769
[Au] Autor:Velázquez F; Grodecki-Pena A; Knapp A; Salvador AM; Nevers T; Croce KJ; Alcaide P
[Ad] Address:Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02111; Sackler School of Biomedical Sciences Immunology Program, Tufts University School of Medicine, Boston, MA 02111; and....
[Ti] Title:CD43 Functions as an E-Selectin Ligand for Th17 Cells In Vitro and Is Required for Rolling on the Vascular Endothelium and Th17 Cell Recruitment during Inflammation In Vivo.
[So] Source:J Immunol;196(3):1305-16, 2016 Feb 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Endothelial E- and P-selectins mediate lymphocyte trafficking in inflammatory processes by interacting with lymphocyte selectin ligands. These are differentially expressed among different T cell subsets and function alone or in cooperation to mediate T cell adhesion. In this study, we characterize the expression and functionality of E-selectin ligands in Th type 17 lymphocytes (Th17 cells) and report that CD43 functions as a Th17 cell E-selectin ligand in vitro that mediates Th17 cell rolling on the vascular endothelium and recruitment in vivo. We demonstrate Th17 cells express CD44, P-selectin glycoprotein ligand (PSGL)-1, and CD43. Few PSGL-1(-/-)CD43(-/-) Th17 cells accumulated on E-selectin under shear flow conditions compared with wild-type cells. CD43(-/-) Th17 cell accumulation on E-selectin was impaired as compared with wild-type and PSGL-1(-/-), and similar to that observed for PSGL-1(-/-)CD43(-/-) Th17 cells, indicating that CD43 alone is a dominant ligand for E-selectin. Notably, this finding is Th17 cell subset specific because CD43 requires cooperation with PSGL-1 in Th1 cells for binding to E-selectin. In vivo, Th17 cell recruitment into the air pouch was reduced in CD43(-/-) mice in response to CCL20 or TNF-α, and intravital microscopy studies demonstrated that CD43(-/-) Th17 cells had impaired rolling on TNF-α-treated microvessels. Furthermore, CD43(-/-) mice were protected from experimental autoimmune encephalomyelitis and had impaired recruitment of Th17 cells in the spinal cord. Our findings demonstrate that CD43 is a major E-selectin ligand in Th17 cells that functions independent of PSGL-1, and they suggest that CD43 may hold promise as a therapeutic target to modulate Th17 cell recruitment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1501171

  4 / 461132 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 26507244
[Au] Autor:Jaworski M; Thome M
[Ad] Address:Department of Biochemistry, University of Lausanne, 1066, Epalinges, Switzerland.
[Ti] Title:The paracaspase MALT1: biological function and potential for therapeutic inhibition.
[So] Source:Cell Mol Life Sci;73(3):459-73, 2016 Feb.
[Is] ISSN:1420-9071
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:The paracaspase MALT1 has a central role in the activation of lymphocytes and other immune cells including myeloid cells, mast cells and NK cells. MALT1 activity is required not only for the immune response, but also for the development of natural Treg cells that keep the immune response in check. Exaggerated MALT1 activity has been associated with the development of lymphoid malignancies, and recently developed MALT1 inhibitors show promising anti-tumor effects in xenograft models of diffuse large B cell lymphoma. In this review, we provide an overview of the present understanding of MALT1's function, and discuss possibilities for its therapeutic targeting based on recently developed inhibitors and animal models.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00018-015-2059-z

  5 / 461132 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 26767933
[Au] Autor:Guidance Development Review Committee; Working Group for Clinical Studies of Cancer Immunotherapy; Working Group for Effector Cell Therapy; Working Group for CMC/Non-clinical Studies; Working Group for Cancer Vaccines and Adjuvants; Working Group for Anti-immune Checkpoint Therapy and Comprehensive Cancer Immunotherapy; Biostatistics Subcommittee
[Ti] Title:2015 Guidance on cancer immunotherapy development in early-phase clinical studies.
[So] Source:Cancer Sci;106(12):1761-71, 2015 Dec.
[Is] ISSN:1349-7006
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The development of cancer immunotherapies is progressing rapidly with a variety of technological approaches. They consist of "cancer vaccines", which are based on the idea of vaccination, "effector cell therapy", classified as passive immunotherapy, and "inhibition of immunosuppression", which intends to break immunological tolerance to autoantigens or immunosuppressive environments characterizing antitumor immune responses. Recent reports showing clinical evidence of efficacy of immune checkpoint inhibitors and adoptive immunotherapies with tumor-infiltrating lymphocytes and tumor-specific receptor gene-modified T cells indicate the beginning of a new era for cancer immunotherapy. This guidance summarizes ideas that will be helpful to those who plan to develop cancer immunotherapy. The aims of this guidance are to discuss and offer important points in early phase clinical studies of innovative cancer immunotherapy, with future progress in this field, and to contribute to the effective development of cancer immunotherapy aligned with the scope of regulatory science. This guidance covers cancer vaccines, effector cell therapy, and inhibition of immunosuppression, including immune checkpoint inhibitors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/cas.12819

  6 / 461132 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 26331453
[Au] Autor:Matsueda S; Shichijo S; Nagata S; Seki C; Yamada A; Noguchi M; Itoh K
[Ad] Address:Cancer Vaccine Center, Kurume University, Kurume, Japan....
[Ti] Title:Identification of novel Lck-derived T helper epitope long peptides applicable for HLA-A2(+) cancer patients as cancer vaccine.
[So] Source:Cancer Sci;106(11):1493-8, 2015 Nov.
[Is] ISSN:1349-7006
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The present study attempted to identify T helper epitope long peptides capable of inducing cytotoxic T lymphocytes (CTL) from Lck antigen (p56(Lck) ), the src family tyrosine kinase, which is known to be aberrantly expressed in metastatic cancers cells, in order to develop a long peptide-based cancer vaccine for HLA-A2(+) cancer patients. Based on the biding motif to the HLA-DR and HLA-A2 alleles, 94 peptides were prepared from the Lck antigen. These peptides were screened for their reactivity to immunoglobulin G (IgG) from plasma of cancer patients, followed by testing of their ability to induce both CD4(+) and CD8(+) T lymphocytes showing not only peptide-specific IFN-γ production but cytotoxicity against HLA-A2(+) cancer cells from peripheral blood mononuclear cells (PBMC) of HLA-A2(+) cancer patients. Among 94 peptides tested, the three T helper epitope long peptides and their inner CTL epitope short peptides with HLA-A2 binding motifs were frequently recognized by IgG of cancer patients, and efficiently induced both CD4(+) IFN-γ(+) and CD8(+) IFN-γ(+) T lymphocytes. Patients' PBMC stimulated with these long peptides showed cytotoxicity against HLA-A2(+) Lck(+) cancer cells in HLA-class I and HLA-class II dependent manners. These three peptides might be useful for long peptide-based vaccines for HLA-A2(+) cancer patients with Lck(+) tumor cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/cas.12805

  7 / 461132 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 24895166
[Au] Autor:Sionov RV; Fridlender ZG; Granot Z
[Ad] Address:Department of Developmental Biology and Cancer Research, Institute for Medical Research Israel Canada, Hebrew University Medical School, 91120, Jerusalem, Israel.
[Ti] Title:The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment.
[So] Source:Cancer Microenviron;8(3):125-58, 2015 Dec.
[Is] ISSN:1875-2292
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Neutrophils are myeloid cells that constitute 50-70 % of all white blood cells in the human circulation. Traditionally, neutrophils are viewed as the first line of defense against infections and as a major component of the inflammatory process. In addition, accumulating evidence suggest that neutrophils may also play a key role in multiple aspects of cancer biology. The possible involvement of neutrophils in cancer prevention and promotion was already suggested more than half a century ago, however, despite being the major component of the immune system, their contribution has often been overshadowed by other immune components such as lymphocytes and macrophages. Neutrophils seem to have conflicting functions in cancer and can be classified into anti-tumor (N1) and pro-tumor (N2) sub-populations. The aim of this review is to discuss the varying nature of neutrophil function in the cancer microenvironment with a specific emphasis on the mechanisms that regulate neutrophil mobilization, recruitment and activation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Da] Date of entry for processing:160115
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1007/s12307-014-0147-5

  8 / 461132 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26391104
[Au] Autor:Arce-Sillas A; Álvarez-Luquín DD; Cárdenas G; Casanova-Hernández D; Fragoso G; Hernández M; Proaño Narváez JV; García-Vázquez F; Fleury A; Sciutto E; Adalid-Peralta L
[Ad] Address:Unidad Periférica para el Estudio de Neuroinflamación del Instituto de Investigaciones Biomédicas de la UNAM en el Instituto Nacional de Neurología y Neurocirugía, México....
[Ti] Title:Interleukin 10 and dendritic cells are the main suppression mediators of regulatory T cells in human neurocysticercosis.
[So] Source:Clin Exp Immunol;183(2):271-9, 2016 Feb.
[Is] ISSN:1365-2249
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Neurocysticercosis is caused by the establishment of Taenia solium cysticerci in the central nervous system. It is considered that, during co-evolution, the parasite developed strategies to modulate the host's immune response. The action mechanisms of regulatory T cells in controlling the immune response in neurocysticercosis are studied in this work. Higher blood levels of regulatory T cells with CD4(+) CD45RO(+) forkhead box protein 3 (FoxP3)(high) and CD4(+) CD25(high) FoxP3(+) CD95(high) phenotype and of non-regulatory CD4(+) CD45RO(+) FoxP3(med) T cells were found in neurocysticercosis patients with respect to controls. Interestingly, regulatory T cells express higher levels of cytotoxic T lymphocyte antigen 4 (CTLA-4), lymphocyte-activation gene 3 (LAG-3), programmed death 1 (PD-1) and glucocorticoid-induced tumour necrosis factor receptor (GITR), suggesting a cell-to-cell contact mechanism with dendritic cells. Furthermore, higher IL-10 and regulatory T cell type 1 (Tr1) levels were found in neurocysticercosis patients' peripheral blood, suggesting that the action mechanism of regulatory T cells involves the release of immunomodulatory cytokines. No evidence was found of the regulatory T cell role in inhibiting the proliferative response. Suppressive regulatory T cells from neurocysticercosis patients correlated negatively with late activated lymphocytes (CD4(+) CD38(+) ). Our results suggest that, during neurocysticercosis, regulatory T cells could control the immune response, probably by a cell-to-cell contact with dendritic cells and interleukin (IL)-10 release by Tr1, to create an immunomodulatory environment that may favour the development of T. solium cysticerci and their permanence in the central nervous system.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/cei.12709

  9 / 461132 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26715756
[Au] Autor:Vivar OI; Masi G; Carpier JM; Magalhaes JG; Galgano D; Pazour GJ; Amigorena S; Hivroz C; Baldari CT
[Ad] Address:Institut Curie, Paris Sciences et Lettres (PSL) Research University, INSERM, Unité 932, Immunité et Cancer, Paris, F-75248, France;...
[Ti] Title:IFT20 controls LAT recruitment to the immune synapse and T-cell activation in vivo.
[So] Source:Proc Natl Acad Sci U S A;113(2):386-91, 2016 Jan 12.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Biogenesis of the immune synapse at the interface between antigen-presenting cells and T cells assembles and organizes a large number of membrane proteins required for effective signaling through the T-cell receptor. We showed previously that the intraflagellar transport protein 20 (IFT20), a component of the intraflagellar transport system, controls polarized traffic during immune synapse assembly. To investigate the role of IFT20 in primary CD4(+) T cells in vitro and in vivo, we generated mice bearing a conditional defect of IFT20 expression in T cells. We show that in the absence of IFT20, although cell spreading and the polarization of the centrosome were unaffected, T-cell receptor (TCR)-mediated signaling and recruitment of the signaling adaptor LAT (linker for activation of T cells) at the immune synapse were reduced. As a consequence, CD4(+) T-cell activation and proliferation were also defective. In vivo, conditional IFT20-deficient mice failed to mount effective antigen-specific T-cell responses, and their T cells failed to induce colitis after adoptive transfer to Rag(-/-) mice. IFT20 is therefore required for the delivery of the intracellular pool of LAT to the immune synapse in naive primary T lymphocytes and for effective T-cell responses in vivo.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1601
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1513601113

  10 / 461132 MEDLINE  
              first record previous record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 26680259
[Au] Autor:Herter JM; Grabie N; Cullere X; Azcutia V; Rosetti F; Bennett P; Herter-Sprie GS; Elyaman W; Luscinskas FW; Lichtman AH; Mayadas TN
[Ad] Address:Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA....
[Ti] Title:AKAP9 regulates activation-induced retention of T lymphocytes at sites of inflammation.
[So] Source:Nat Commun;6:10182, 2015.
[Is] ISSN:2041-1723
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The mechanisms driving T cell homing to lymph nodes and migration to tissue are well described but little is known about factors that affect T cell egress from tissues. Here, we generate mice with a T cell-specific deletion of the scaffold protein A kinase anchoring protein 9 (AKAP9) and use models of inflammatory disease to demonstrate that AKAP9 is dispensable for T cell priming and migration into tissues and lymph nodes, but is required for T cell retention in tissues. AKAP9 deficiency results in increased T cell egress to draining lymph nodes, which is associated with impaired T cell re-activation in tissues and protection from organ damage. AKAP9-deficient T cells exhibit reduced microtubule-dependent recycling of TCRs back to the cell surface and this affects antigen-dependent activation, primarily by non-classical antigen-presenting cells. Thus, AKAP9-dependent TCR trafficking drives efficient T cell re-activation and extends their retention at sites of inflammation with implications for disease pathogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1512
[Cu] Class update date: 160123
[Lr] Last revision date:160123
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/ncomms10182


page 1 of 46114 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