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  • Lee, Kyoo-A  (5)
  • English  (5)
  • 2010-2014  (5)
  • Medicine  (5)
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  • English  (5)
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  • 2010-2014  (5)
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  • Medicine  (5)
RVK
  • 1
    Online Resource
    Online Resource
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 1_Supplement ( 2011-04-01), p. 152.16-152.16
    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
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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  • 2
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 22 ( 2014-11-15), p. 6705-6716
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 22 ( 2014-11-15), p. 6705-6716
    Abstract: Extramedullary myelopoiesis occurs commonly in tumor-bearing animals and is known to lead to accumulation of peripheral myeloid-derived suppressor cells (MDSC), which play an important role in immune escape. However, the cellular and molecular mechanisms by which tumors induce extramedullary myelopoiesis are poorly understood. In this study, we found that osteopontin expressed by tumor cells enhances extramedullary myelopoiesis in a CD44-dependent manner through the Erk1/2–MAPK pathway. Osteopontin-mediated extramedullary myelopoiesis was directly associated with increased MDSCs in tumor-bearing hosts. More importantly, osteopontin silencing in tumor cells delayed both tumor growth and extramedullary myelopoiesis, while the same treatment did not affect tumor growth in vitro. Finally, treatment with an antibody against osteopontin inhibited tumor growth and synergized with cell-based immunotherapeutic vaccines in mediating antitumor immunity. Our findings unveil a novel immunosuppressive role for tumor-derived osteopontin and offer a rationale for its therapeutic targeting in cancer treatment. Cancer Res; 74(22); 6705–16. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
    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
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 1491907-2
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  • 4
    Online Resource
    Online Resource
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 1_Supplement ( 2011-04-01), p. 107.4-107.4
    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
    RVK:
    RVK:
    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
    The American Association of Immunologists ; 2014
    In:  The Journal of Immunology Vol. 192, No. 1_Supplement ( 2014-05-01), p. 65.17-65.17
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 192, No. 1_Supplement ( 2014-05-01), p. 65.17-65.17
    Abstract: T cells, which are major components of adaptive immune system, are dysfunctional in aged individuals due to numerous intrinsic and extrinsic changes of aged T cell. Recently, several studies have shown that the expression of inhibitory receptors is increased on CD8 T cells from aged mice, which is also observed on exhausted CD8 T cells in chronic infection model, by which effector T cells are negatively regulated. In this study, we described that Tim-3+ PD-1+ CD8 T cells increased in aged mice compared to those of young mice. The more extensive investigations on the functional characteristics of aged Tim-3+ PD-1+ CD8 T cell revealed that these cells had defects in cytokine (IFN-γ, TNF-α) production and proliferation, consistent with features of exhausted CD8 T cell in a chronic infection model. Aged Tim-3+ PD-1+ CD8 T cell produced more immune regulatory cytokine, IL-10, than PD-1 single positive or Tim-3 and PD-1 double negative CD8 T cells. Furthermore, there was more diminished homeostatic proliferation of aged Tim-3+ PD-1+ CD8 T cells than other subsets in lymphopenic conditions, indicating that aged Tim-3+ PD-1+ CD8 T cell had cell-intrinsic defect in proliferation capacity. Interestingly, adoptively transferred aged Tim-3+ PD-1+ CD8 T cells in naïve B6 hosts survived longer than other subsets. Collectively, our findings on aged Tim-3+ PD-1+ CD8 T cell would provide a important insight for understanding the defect in the immune senescence.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2014
    detail.hit.zdb_id: 1475085-5
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