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  • Lee, Kyoo-A  (6)
  • Lee, Yoon-Sook  (6)
  • English  (6)
  • Medicine  (6)
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  • English  (6)
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  • Medicine  (6)
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  • 1
    Online Resource
    Online Resource
    [alpha]-GalCer analogues with branched acyl chain enhance humoral and cellular immune responses in a nasal influenza vaccine (132.11)
    The American Association of Immunologists ; 2009
    In:  The Journal of Immunology Vol. 182, No. 1_Supplement ( 2009-04-01), p. 132.11-132.11
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 132.11-132.11
    Abstract: α-galactosylceramide (α-GalCer) can act as a safe and effective adjuvant for a nasal vaccine that induces protective immune responses against tumors and viral infections. In this study, α-GalCer analogues were designed to have branched acyl chain by modification of their fatty acyl chain based on the CD1d/glycolipid structures. Two α-GalCer analogues with various branched chain lengths; LDH-II-28 and LDH-II-30 were prepared and evaluated for their efficacy as a nasal influenza vaccine adjuvant. These analogues displayed improved solubility over α-GalCer and effectively stained NKT cells both in mouse and human. They also potently stimulated NKT cells to exhibit different cytokine release profiles from α-GalCer in vitro and in vivo. When profiling serum cytokines in vivo, LDH-II-30 provoked both Th1/Th2 cytokines, while LDH-II-28 induced more Th2-biased cytokine release with diminished IFN-γ production. We found that single immunization of inactivated influenza virus A/PR/8/34 (PR8) together with α-GalCer analogues enhanced PR8-specific humoral and cellular immune responses in both systemic and mucosal compartments. Notably, LDH-II-30 exhibited potent adjuvant effects with significantly higher systemic IgG, mucosal sIgA Ab titers and enhanced CTL generation compared to immunization with inactivated PR8 alone, while addition of LDH-II-28 to inactivated PR8 only marginally increased PR8-specific immune responses. These results suggest that α-GalCer analogues with branched acyl chain could be used as an effective mucosal adjuvant for the induction of influenza vaccine-specific humoral and cellular immune responses.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.182.Supp.132.11
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2009
    detail.hit.zdb_id: 1475085-5
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  • 2
    Online Resource
    Online Resource
    4-1BB Engagement Costimulates NKT Cell Activation and Exacerbates NKT Cell Ligand-Induced Airway Hyperresponsiveness and Inflammation
    The American Association of Immunologists ; 2008
    In:  The Journal of Immunology Vol. 180, No. 4 ( 2008-02-15), p. 2062-2068
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 180, No. 4 ( 2008-02-15), p. 2062-2068
    Abstract: Multiple studies have demonstrated that 4-1BB (CD137), a member of the TNF receptor superfamily, is expressed on several immune cells including activated T cells. However, the expression and the role of 4-1BB on natural killer T (NKT) cells have not been fully characterized. In this study, it was shown that 4-1BB was not expressed on naive NKT cells but was rapidly induced on activated NKT cells by TCR engagement with α-galactosylceramide (α-GalCer). Also, 4-1BB signaling provided by 3H3, an agonistic anti-4-1BB mAb, promoted NKT cell activation resulting in enhanced cytokine production of NKT cells driven by α-GalCer. When NKT cell-driven airway immune responses were evaluated by intranasal administration of α-GalCer, airway hyperresponsiveness (AHR) and lung inflammation were significantly more aggravated in mice treated with 3H3 and α-GalCer than in mice treated with α-GalCer alone. These aggravations were accompanied by up-regulation of IL-4, IL-13, and IFN-γ production. Interestingly, AHR was not developed in IL-4Rα-deficient mice treated with α-GalCer with or without 3H3 but was exacerbated in IFN-γ-deficient mice. Our study suggests that 4-1BB on NKT cells functions as a costimulatory molecule and exacerbates the induction of NKT cell-mediated AHR, which is dependent on the IL-4Rα-mediated pathway.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.180.4.2062
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2008
    detail.hit.zdb_id: 1475085-5
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  • 3
    Online Resource
    Online Resource
    A distinct subset of natural killer T cells produces IL-17, contributing to airway infiltration of neutrophils but not to airway hyperreactivity
    Elsevier BV ; 2008
    In:  Cellular Immunology Vol. 251, No. 1 ( 2008), p. 50-55
    Details
    In: Cellular Immunology, Elsevier BV, Vol. 251, No. 1 ( 2008), p. 50-55
    Type of Medium: Online Resource
    ISSN: 0008-8749
    URL: Article
    DOI: 10.1016/j.cellimm.2008.03.004
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2008
    detail.hit.zdb_id: 1462601-9
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  • 4
    Online Resource
    Online Resource
    Secreted Frizzled-related protein-1 regulates human peripheral CD4 T cell responses (152.16)
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 1_Supplement ( 2011-04-01), p. 152.16-152.16
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 1_Supplement ( 2011-04-01), p. 152.16-152.16
    Abstract: Secreted Frizzled-related protein-1 (sFRP1) has been described as a modulator for complex Wnt signaling pathway. In addition to its essential function in T cell development, recent studies have indicated a critical role for Wnt/β-catenin signaling pathway in the biology of mature T cells such as differentiation, polarization, and survival. Here, we investigated the effect of sFRP1 on TCR/CD28 stimulated memory and naive CD4 T cells derived from human peripheral blood in the context of cytokine response of Th subsets. sFRP1 treatment inhibited proliferation and early cytokine secretion of CD3/CD28 activated memory CD4(+)CD45RO(+) T cells, whereas it increased proliferation of CD3/CD28 activated naïve CD4(+)CD25(-)CD45RO(-) T cells. Moreover, sFRP1 influenced lineage choice of naïve CD4 T cells, resulting in enhanced Th1 and Th17 polarization with suppressed Th2 fate. Regulation of Th1/Th2 polarization by sFRP1 was expected from its antagonistic effect on Wnt/β-catenin signaling reported to favor Th2 over Th1 polarization in CD4 T cells. Interestingly, sFRP1 also positively regulated Th17 polarization and sFRP1 treatment of naïve CD4 T cells in Th17-polarizing conditions up-regulated IL-17 expression. Taken together, our observations suggest the function of sFRP1 in the control of activated human peripheral CD4 T cell subsets.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.186.Supp.152.16
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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  • 5
    Online Resource
    Online Resource
    Retinoic acid alleviates Con A-induced hepatitis and differentially regulates effector production in NKT cells : Highlights
    Wiley ; 2012
    In:  European Journal of Immunology Vol. 42, No. 7 ( 2012-07), p. 1685-1694
    Details
    In: European Journal of Immunology, Wiley, Vol. 42, No. 7 ( 2012-07), p. 1685-1694
    Type of Medium: Online Resource
    ISSN: 0014-2980
    URL: Issue
    URL: Article
    DOI: 10.1002/eji.v42.7
    DOI: 10.1002/eji.201142322
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 1491907-2
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  • 6
    Online Resource
    Online Resource
    Retinoic acid ameliorates experimental autoimmune hepatitis and suppresses the production of cytokine in NKT cells in mice (107.4)
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 1_Supplement ( 2011-04-01), p. 107.4-107.4
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 1_Supplement ( 2011-04-01), p. 107.4-107.4
    Abstract: Retinoic acid(RA) has been demonstrated as a critical regulator of various immune cells. Especially RA regulates the response of helper T cells skewing to Th2 response during the priming. In spite of abundant studies regarding T cells, the role of RA on natural killer T(NKT) cell mediated response has not been assessed. In the present study, we demonstrated the effect of RA on the experimental autoimmune hepatitis and the response of NKT cells. We first examined whether pretreatment of RA could regulate concanavlin A(Con A)-induced hepatitis, which is initiated by NKT cells. The survival rate was increased dramatically and liver damage was ameliorated when RA was pretreated. And also the levels of IFN-gamma and IL-4 in serum were both reduced significantly in RA treated group and the cytokine expressing cells were reduced in various lymphocytes in liver, especially in NKT cells. Cytokine suppressive effects of RA were observed when NKT cell specific ligand was treated. These regulations were also detected when mononuclear cells of liver or splenocytes were treated with the stimulants in the presence of RA in vitro. These regulations are not related with the early activation of NKT cells. Rather, the apoptosis of lymphocytes in liver after the administration of con A were increased in RA-treated group. These findings implicates that RA ameliorates NKT cell mediated hepatitis and it could be used clinically to liver injury related with NKT cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.186.Supp.107.4
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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