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  1. AU="Donald Bellgrau"
  2. AU=Shorter Edward
  3. AU=Pham Minh Tan
  4. AU="Caniglia, John L"
  5. AU="Rao, Jiajia"
  6. AU="Vincent, Steve"
  7. AU="Oguntade, Habibat A"
  8. AU="Shah, Nikita Chetan"
  9. AU="Usherwood, Tim"
  10. AU="Petr Kala"
  11. AU=Talmage David A
  12. AU="Alessandro Achilli"
  13. AU="Julià Blanco"
  14. AU=Pardee Arthur B
  15. AU="Moossy, John J"
  16. AU="Ledger, Elizabeth V"
  17. AU="Abichandani, Deepa"
  18. AU="Piccinelli, Fabio"
  19. AU="Malinova, Tsveta S"
  20. AU="Harwood, Janet"
  21. AU=Buscombe John R
  22. AU=Meyer-Rusenberg Birthe
  23. AU="Jiang, Weiyan"
  24. AU="Mills, W"
  25. AU="Pintó, Rosa M."
  26. AU="Voisin, Tiphaine"
  27. AU="Takahashi, Hiromi"
  28. AU="Lin, Johnny"
  29. AU="Lee, Yu-Ru"
  30. AU="Safrankova, J."
  31. AU="Lanting, Linda L"
  32. AU=Koushik Nikhil S
  33. AU="Culhane, John"
  34. AU="Chippada, Appa Rao"
  35. AU="Hiroki Sato" AU="Hiroki Sato"
  36. AU="Al-Amer Eshraq"
  37. AU="Thanacoody, Ruben"
  38. AU="Lin, Chi-Wei"
  39. AU="Chidambaram, Vignesh"

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  1. Artikel ; Online: Nfatc2 and Tob1 have non-overlapping function in T cell negative regulation and tumorigenesis.

    Sarah L May / Qing Zhou / Mitzi Lewellen / Cristan M Carter / David Coffey / Steven L Highfill / Christoph M Bucher / Ilze Matise / Herbert C Morse / M Gerard O'Sullivan / Melissa Schutten / Charles Johnson / Donald Bellgrau / Bruce R Blazar / Jaime F Modiano

    PLoS ONE, Vol 9, Iss 6, p e

    2014  Band 100629

    Abstract: Nfatc2 and Tob1 are intrinsic negative regulators of T cell activation. Nfatc2-deficient and Tob1-deficient T cells show reduced thresholds of activation; however, whether these factors have independent or overlapping roles in negative regulation of T ... ...

    Abstract Nfatc2 and Tob1 are intrinsic negative regulators of T cell activation. Nfatc2-deficient and Tob1-deficient T cells show reduced thresholds of activation; however, whether these factors have independent or overlapping roles in negative regulation of T cell responses has not been previously examined. Here, we show that Nfatc2 knockout (KO) but not Tob1 KO mice have age-associated accumulation of persistently activated T cells in vivo and expansion of the CD44+ memory cell compartment and age-associated lymphocytic infiltrates in visceral organs, without significant changes in numbers of CD4+CD25+Foxp3+ regulatory T cells (Treg). In vitro, CD4+CD25- "conventional" T cells (Tconvs) from both KO strains showed greater proliferation than wild type (WT) Tconvs. However, while Tregs from Nfatc2 KO mice retained normal suppressive function, Tregs from Tob1 KOs had enhanced suppressive activity. Nfatc2 KO Tconvs expanded somewhat more rapidly than WT Tconvs under conditions of homeostatic proliferation, but their accelerated growth capacity was negated, at least acutely, in a lymphoreplete environment. Finally, Nfatc2 KO mice developed a previously uncharacterized increase in B-cell malignancies, which was not accelerated by the absence of Tob1. The data thus support the prevailing hypothesis that Nfatc2 and Tob1 are non-redundant regulators of lymphocyte homeostasis.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2014-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: A whole recombinant yeast-based therapeutic vaccine elicits HBV X, S and Core specific T cells in mice and activates human T cells recognizing epitopes linked to viral clearance.

    Thomas H King / Charles B Kemmler / Zhimin Guo / Derrick Mann / Yingnian Lu / Claire Coeshott / Adam J Gehring / Antonio Bertoletti / Zi Z Ho / William Delaney / Anuj Gaggar / G Mani Subramanian / John G McHutchison / Shikha Shrivastava / Yu-Jin L Lee / Shyamasundaran Kottilil / Donald Bellgrau / Timothy Rodell / David Apelian

    PLoS ONE, Vol 9, Iss 7, p e

    2014  Band 101904

    Abstract: Chronic hepatitis B infection (CHB) is characterized by sub-optimal T cell responses to viral antigens. A therapeutic vaccine capable of restoring these immune responses could potentially improve HBsAg seroconversion rates in the setting of direct acting ...

    Abstract Chronic hepatitis B infection (CHB) is characterized by sub-optimal T cell responses to viral antigens. A therapeutic vaccine capable of restoring these immune responses could potentially improve HBsAg seroconversion rates in the setting of direct acting antiviral therapies. A yeast-based immunotherapy (Tarmogen) platform was used to make a vaccine candidate expressing hepatitis B virus (HBV) X, surface (S), and Core antigens (X-S-Core). Murine and human immunogenicity models were used to evaluate the type and magnitude of HBV-Ag specific T cell responses elicited by the vaccine. C57BL/6J, BALB/c, and HLA-A*0201 transgenic mice immunized with yeast expressing X-S-Core showed T cell responses to X, S and Core when evaluated by lymphocyte proliferation assay, ELISpot, intracellular cytokine staining (ICS), or tumor challenge assays. Both CD4+ and CD8+ T cell responses were observed. Human T cells transduced with HBc18-27 and HBs183-91 specific T cell receptors (TCRs) produced interferon gamma (IFNγ following incubation with X-S-Core-pulsed dendritic cells (DCs). Furthermore, stimulation of peripheral blood mononuclear cells (PBMCs) isolated from CHB patients or from HBV vaccine recipients with autologous DCs pulsed with X-S-Core or a related product (S-Core) resulted in pronounced expansions of HBV Ag-specific T cells possessing a cytolytic phenotype. These data indicate that X-S-Core-expressing yeast elicit functional adaptive immune responses and supports the ongoing evaluation of this therapeutic vaccine in patients with CHB to enhance the induction of HBV-specific T cell responses.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2014-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  3. Artikel ; Online: A 9L Gliosarcoma Transplantation Model for Studying Adoptive Immunotherapy into the Brains of Conscious Rats

    Monika Fleshner / Linda R. Watkins / Joan M. Redd / Carol A Kruse / Donald Bellgrau

    Cell Transplantation, Vol

    1992  Band 1

    Abstract: A rat model for brain tumor immunotherapy is described that closely mimics the type of treatment that could be administered to humans. It involves surgical implantation of a permanent cannula in the brain, through which tumor cells and various effector ... ...

    Abstract A rat model for brain tumor immunotherapy is described that closely mimics the type of treatment that could be administered to humans. It involves surgical implantation of a permanent cannula in the brain, through which tumor cells and various effector cells and/or cytokines can be injected. The advantage of this system over more conventional animal surgical procedures is that conscious animals can be treated multiple times while avoiding morbidity and mortality associated with reoperative procedures. Using this system to study adoptive immunotherapy for brain tumors, we provide evidence that the 9L gliosarcoma tumor from the Fischer rat strain can be reduced or destroyed in situ following adoptive immunotherapy with specifically activated cytotoxic T lymphocytes.
    Schlagwörter Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 1992-07-01T00:00:00Z
    Verlag SAGE Publishing
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

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