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  • The American Association of Immunologists  (5)
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  • The American Association of Immunologists  (5)
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  • 1
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 166, No. 2 ( 2001-01-15), p. 787-794
    Kurzfassung: The down-regulation of surface expression of MHC class I molecules has recently been reported in the CD99-deficient lymphoblastoid B cell line displaying the characteristics of Hodgkin’s and Reed-Sternberg phenotype. Here, we demonstrate that the reduction of MHC class I molecules on the cell surface is primarily due to a defect in the transport from the Golgi complex to the plasma membrane. Loss of CD99 did not affect the steady-state expression levels of mRNA and protein of MHC class I molecules. In addition, the assembly of MHC class I molecules and the transport from the endoplasmic reticulum to the cis-Golgi occurred normally in the CD99-deficient cells, and no difference was detected between the CD99-deficient and the control cells in the pattern and degree of endocytosis. Instead, the CD99-deficient cells displayed the delayed transport of newly synthesized MHC class I molecules to the plasma membrane, thus causing accumulation of the molecules within the cells. The accumulated MHC class I molecules in the CD99-deficient cells were colocalized with α-mannosidase II and γ-adaptin in the Golgi compartment. These results suggest that CD99 may be associated with the post-Golgi trafficking machinery by regulating the transport to the plasma membrane rather than the endocytosis of surface MHC class I molecules, providing a novel mechanism of MHC class I down-regulation for immune escape.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2001
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Online-Ressource
    Online-Ressource
    The American Association of Immunologists ; 2013
    In:  The Journal of Immunology Vol. 190, No. 1_Supplement ( 2013-05-01), p. 207.7-207.7
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 190, No. 1_Supplement ( 2013-05-01), p. 207.7-207.7
    Kurzfassung: Clonorchis sinensis (C. sinensis) infection is known to cause cholangiocarcinomas in humans, but the mechanism is not clearly understood. In order to verify the role of excretory/secretory products (ESP) from C. sinensis in cell proliferation and the modulation of cancer related molecules, HEK293T cells were cultured with ESP and/or NDMA (N-nitrosodimethylamine), and then the mode of cell cycle and the expression of proteins were analyzed by using FACS, western blotting and confocal analysis. When the ESP of C. sinensis and NDMA were treated, the degree of cell proliferation was upregulated and the proportion of G2/M phase cells were increased by 25%-30% as compared with that of control. The expression pattern of the cell cycle proteins was also changed when both ESP and NDMA were added. Theses indicate that ESP from C. sinensis and NDMA synergistically affected the regulation of cell cycle proteins. In addition, the levels of Cox-2 and connexin 43 (Cx43) which is known as cancer related gap junction protein were upregulated by the addition of ESP and NDMA in vivo. In addition, the level of another gap junction protein, Cx32, which is also known as cancer inhibitor was down- regulated. Our results suggest that exposure to C. sinensis and a small amount of NDMA promote uncontrolled cellular proliferation of the bile duct epithelial cells and the upregulation of cancer related intracellular molecules.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2013
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    Online-Ressource
    Online-Ressource
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 1_Supplement ( 2012-05-01), p. 112.3-112.3
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 1_Supplement ( 2012-05-01), p. 112.3-112.3
    Kurzfassung: Clonorchis sinensis (C. sinensis), one of liver flukes, can cause chronic infection while they reside in the bile duct and leads to cholangiocarcinoma in humans. We investigated interaction between live C. sinensis worm and murine macrophage cell line, RAW264.7, using a non contact co-culture transwell plate. The results shown that the worms are able to activate RAW cells to express surface TLR4 and to promote IL-10 and TGF-β secretion. There are minor differences between direct and indirect exposure of the worms. As we hypothesized that anti-oxidant enzyme produced by C. sinensis might stimulate host immune reactions, we cloned antioxidant enzyme, Thioredoxin peroxidase (TPX, 2-Cys peroxidase), and the recombinant protein (rTPX) has been produced by using the bacterial system. Mouse macrophage cells, RAW264.7 cells, were treated with rTPX and checked the level of cell surface markers. We found that expression of TLR4 and CD40 molecules were augmented at 3 and 6 hours time points, respectively. Surface expression of TLR4 was prolonged up to 48 hrs, while CD40 was temporarily expressed. ELISA results showed that IL-4 level was slightly down-regulated by TPX treatment, however, IL-10 secretion was increased and even doubled when IL-4 and TPX were treated together. Although, more than one molecule could be involved in antigenicity of C. sinensis, we report here that the TPX from C. sinensis is a candidate that acts as “infection alarm” to awake the host innate immune cells.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2012
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 4
    Online-Ressource
    Online-Ressource
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 1_Supplement ( 2012-05-01), p. 164.22-164.22
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 1_Supplement ( 2012-05-01), p. 164.22-164.22
    Kurzfassung: The current knowledge of immunological response to clonorchiasis, a major Asian endemic helminthic disease, is insufficient. To develop a mouse model of clonorchiasis, CBA/N and C57BL/6 mice were infected with Clonorchis sinensis metacercariae and analyzed host responses at 2, 4, and 8 weeks post infection. CBA/N mice infected with C. sinensis developed more severe gross and histopathological changes than C57BL/6 mice. In addition, more pronounced inflammatory cell infiltration and hepatocyte necrosis were noticed in CBA/N mice, especially at 2 weeks post-infection. Serum biomarkers of liver injury (ALT and AST) were increased significantly in CBA/N mice after C. sinensis infection as compared with those of C57BL/6 mice. We also analyzed the proliferation of splenocytes stimulated with crude C. sinensis antigen and cytokine production in the culture supernatant of activated splenocytes. We found that splenocytes from CBA/N mice were highly proliferative and the IL-17 level was increased. Additionally, an increased IL-4 level was sustained until 8 weeks post-infection in CBA/N mice. The serum levels of C. sinensis-specific IgG1 and IgG2a were increased in CBA/N mice, whereas IgE was increased in C57BL/6 mice. Furthermore, the level of IL-17 was increased in intrahepatic lymphocytes in CBA/N infected groups. Present study suggest that CBA/N could be a appropriate mouse model for clonorchiasis and might be useful for studying early immune responses in liver fluke infection.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2012
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 5
    Online-Ressource
    Online-Ressource
    The American Association of Immunologists ; 2015
    In:  The Journal of Immunology Vol. 194, No. 1_Supplement ( 2015-05-01), p. 202.14-202.14
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 194, No. 1_Supplement ( 2015-05-01), p. 202.14-202.14
    Kurzfassung: Clonorchis sinensis (C. sinensis) estabilishes long term parasitism within bile ducts without notable symptoms. General down-modulated host immune responses in helminth infestation are maintained by excretory-secretory products (ESP), produced by the live parasites and considered as an important immunomodulator in this context. Reference based study found out that Thioredoxin peroxidase (TPX) of helminth parasites had an immune-modulating property toward Th2 type through induction of regulatory phenotype of macrophages. Hence, full length of TPX and a number of recombinant TPX fragments of C. sinensis were produced by using bacteria system. The CS-TPX was able to inhibit LPS-induced surface expression of TLR4 in mouse macrophage cell line, RAW264.7, and LPS-induced secretion of pro-inflammatory mediators NO, TNF-α and IL-6. Moreover, CS-TPX induces IL-10, but not TGF-β. Pull-down assay results revealed that the direct interaction between CS-TPX and TLR4 protein. Furthermore, we found that the smallest recombinant fragment of CS-TPX, which is T44, has comparable anti-inflammatory property as compared with full length CS-TPX. In conclusion, present study describes the macrophage regulatory function of C. sinensis ESP and the smallest fragment of CS-TPX, T44, could function of the negative regulator in LPS treated macrophage cell line RAW264.7 cells. Defined CS-TPX T44 will be one of the best candidates for therapeutic immunosuppressant in allergies and autoimmune diseases.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2015
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
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