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  • Medicine  (4)
  • 1
    Online Resource
    Online Resource
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 84.10-84.10
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 84.10-84.10
    Abstract: Intestinal intraepithelial lymphocytes (IELs) are a various community of lymphoid cells located in between the intestinal epithelial cells (IECs) that configure the intestinal mucosal barrier. The epithelial γδT cells act as a major T cell population in epithelia, which is support in tissue homeostasis and repair. However, we found that the γδT cell population was strikingly increased in IELs in TAM receptor-deficient mice. Based on these data, we tested whether this receptor acts as a crucial regulator, which may generate better homing to the intestinal epithelium. We also tested that adoptive transfer of γδT cells to show γδT cell homing to the intestinal epithelium. Our study shows that a key factor in γδT cell homing into the intestinal epithelium, to maintain homeostasis.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 2
    Online Resource
    Online Resource
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 232.10-232.10
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 232.10-232.10
    Abstract: Salmonella Typhimurium (S. Typhimurium), one of the most common infectious bacteria, triggers an inflammatory reaction in epithelial cells of the intestine and migrates into the spleen and liver to colonize. To elucidate the role of Axl in bacterial infection-mediated inflammatory responses, Axl-depleted mice and WT mice were infected with S. Typhimurium, and the systemic dissemination caused by the infection was evaluated. The Axl-depleted mice shows better histological scores and increased intraepithelial T cells. The colony number and CFU of S. typhimurium were also lower in the liver of Axl-depleted mice than in that of WT mice. Thus, lack of Axl results in better resistance to S. Typhimurium, suggesting that downregulation of Axl is essential for bacterial resistance by inducing increased number and activity of intraepithelial T cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    The American Association of Immunologists ; 2013
    In:  The Journal of Immunology Vol. 190, No. 1_Supplement ( 2013-05-01), p. 43.15-43.15
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 190, No. 1_Supplement ( 2013-05-01), p. 43.15-43.15
    Abstract: The role of TREM2 in adipogenesis and obesity has not yet been defined. Here, we report that TREM2-transgenic (TG) mice were much more obese than wild-type mice after feeding with a high-fat diet (HFD), independent of the quantity of food intake. These HFD-fed TREM2 TG mice manifested adipocyte hypertrophy, glucose and insulin resistance and hepatic steatosis. The expression of adipogenic regulator genes, such as peroxisome proliferator-activated receptor γ, CCAAT/enhancer-binding protein α, fatty-acid synthase and CD36, was markedly increased in the epididymal white adipose tissue (EWAT) of the HFD-fed TG mice. In addition, the EWAT of the HFD-fed TG mice exhibited decreased Wnt10b expression and increased GSK-3β-mediated β-catenin phosphorylation. In contrast, the blockade of TREM2 signaling using TREM2-Ig resulted in the inhibition of adipocyte differentiation in vitro and a reduction in body weight in vivo by downregulating the expression of adipogenic regulators. Taken together, these results suggested that TREM2 induces obesity by promoting adipogenesis via the upregulation of adipogenic regulators in conjunction with the Wnt10b/β-catenin signaling pathway.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2013
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    The American Association of Immunologists ; 2009
    In:  The Journal of Immunology Vol. 182, No. 1_Supplement ( 2009-04-01), p. 88.13-88.13
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 88.13-88.13
    Abstract: To elucidate the role of Axl on the regulation of LIGHT expression, we established the stably over-expressing Axl T lymphoma cells in mouse EL4 (EL4-Axl) and human Jurkat T lymphoma cells (Jurkat-Axl). The expression of LIGHT and its receptor, herpes virus entry mediator (HVEM) was remarkably increased both in EL4-Axl and Jurkat-Axl compared with the individual controls. Furthermore, the expression of LIGHT, HVEM and IFN-γ was reduced in the various tissues of Axl-/- mice. The proliferation of EL4-Axl cells was inhibited by treatment of Axl-Ig in a concentration and LIGHT expression-dependent manner. In LIGHT promoter assay using a transient transfection of Jurkat-Axl cells with 5¡ deletion mutants, luciferase reporter activity showed the highest transcriptional activity in the gene segment -190/+1. Electrophoretic mobility shift assay (EMSA) and Western blot analysis revealed that Sp1 was able to directly bind to its binding site on LIGHT promoter upon triggering AKT/PI3K signaling pathway. These results suggest that Sp1 plays a crucial role in the regulation of LIGHT expression by Axl signaling in T lymphoma. This work was supported by the SRC/ERC program of MOST/KOSEF (RESEARCH CENTER FOR WOMEN'S DISEASES)
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2009
    detail.hit.zdb_id: 1475085-5
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