Sungyoo Cho

Indiana University-Purdue University Indianapolis, Indianapolis, IN, United States

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Publications (7)34.36 Total impact

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    ABSTRACT: CD1d molecules are MHC class I-like molecules that present lipids to a unique subpopulation of T cells called NKT cells. The cytoplasmic tail of human CD1d possesses a tyrosine-based endosomal targeting motif (YXXZ). As such, these molecules traffic through the endocytic pathway, where it is believed that they are loaded with the antigenic lipid that stimulates NKT cells. In the current study, it was found that the T322 residue in the human CD1d tail is a major signal controlling transport to the cell surface and thus its functional expression. Mimicking the phosphorylation of this residue or removal of the entire cytoplasmic tail negates its ability to regulate CD1d trafficking, resulting in lysosomal targeting and degradation. These results demonstrate an important role of a heretofore unknown signal in the cytoplasmic tail of CD1d that may have relevance to other type I integral membrane proteins that traverse through the endocytic pathway.
    The Journal of Immunology 04/2010; 184(9):4973-81. · 5.52 Impact Factor
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    ABSTRACT: The HIV-1 Nef protein causes a decrease in major histocompatibility complex (MHC) class I and CD4 molecule expression on the cell surface. To determine if Nef can affect components of the innate immune response, we assessed the ability of Nef to alter the cell surface expression of human CD1d. In cells co-expressing CD1d and Nef, a substantial reduction in the cell surface level of CD1d was observed, with a concomitant reduction in the activation of CD1d-restricted NKT cells. Nef had a minimal effect on the cell surface expression of a mutant CD1d molecule in which the last 6 or 10 amino acids of the cytoplasmic tail were deleted. Additionally, it was found that Nef physically interacted with wild-type (but not tail-deleted) CD1d. Therefore, one means by which HIV-1 may be able to establish a foothold in an infected individual is by directly interfering with the functional cell surface expression of CD1d.
    Virology 08/2005; 337(2):242-52. · 3.37 Impact Factor
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    ABSTRACT: CD1d is an MHC class I-like surface molecule that presents endogenous glycoplipid antigens. The effect of HIV infection on CD1d surface expression has not yet been reported. FACS analysis revealed significantly lower levels of CD1d on CD14(+) monocytes from HIV-infected subjects compared to HIV-infected subjects on HAART and healthy controls. CD1d expression correlated inversely with viral load in infected individuals. CD1d surface expression on human cell lines was downregulated after infection with M-tropic HIV, T-tropic HIV, or after exposure to HIV gp120 in vitro. These data suggest that CD1d-mediated responses are altered during HIV infection and may thus contribute to the global immunodeficiency seen in these patients.
    Immunology Letters 05/2005; 98(1):131-5. · 2.34 Impact Factor
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    ABSTRACT: NKT cell activation plays an important role in regulating innate and adaptive immunity during infection. We have previously found that there is a dramatic reduction in the NKT cell population on day 3 after an acute lymphocytic choriomeningitis virus (LCMV) infection. In this study, we report that this loss continued for at least 3 months and was not simply due to internalization of the TCR. Concomitant with the decrease in NKT cells was an increase in the percentage of Annexin V(+) NKT cells that remained in vivo, suggesting that the reduction in NKT cells at these late stages post-infection occurred by activation-induced cell death. Interestingly, APC from LCMV-infected mice could activate NKT cells in vitro at higher levels than those from uninfected mice and was concomitant with an increase in apoptosis in NKT cells. However, this could not be blocked by mAb to murine CD1d, and APC from LCMV-infected (but not uninfected) CD1d1-deficient mice could also stimulate NKT cells. Collectively, our data suggest that the activation and subsequent long-term loss of NKT cells is a normal component of the host's antiviral immune response, and this occurs in a CD1d-independent manner.
    European Journal of Immunology 04/2005; 35(3):879-89. · 4.97 Impact Factor
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    ABSTRACT: CD11b, CD11c, and F4/80 are normally used to define dendritic cell and/or macrophage populations. In this study, the expression of all three markers was observed on CD8(+) T cells following infection of mice with several distinct viruses. Using lymphocytic choriomeningitis virus as a model virus, it was found that relatively more CD11b(+)CD8(+) and CD11c(+)CD8(+) T cells were present in the periphery than in primary lymphoid organs; in contrast, the F4/80(+)CD8(+) T cell population was more prevalent in the spleen. All three myeloid markers were detected on virus-specific CTL. The expression of CD11b and CD11c on CD8(+) T cells correlated with their level of CTL activity, whereas the F4/80(+)CD8(+) T cell population increased after the peak of the CTL response but did not have higher CTL activity. These data suggest that there is a differential induction of CD11b, CD11c, and F4/80 on virus-specific CD8(+) T cells following an acute virus infection.
    European Journal of Immunology 11/2003; 33(10):2736-43. · 4.97 Impact Factor
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    ABSTRACT: CD1d molecules are lipid antigen-presenting molecules. They are involved in presenting these antigens to a unique subpopulation of T cells called natural killer T (NKT) cells, which have the capacity to produce both T helper (Th) 1 and Th2 cytokines. Thus, it is possible that the antigens presented by CD1d and/or the level at which they are presented could have profound effects on the immunoregulation of autoimmune and infectious diseases, as well as cancer. Because of the ability of CD1d-binding ligands to modulate NKT cell responses, targeting CD1d-mediated antigen presentation as a novel approach for new therapies in these and other diseases holds great promise.
    Critical Reviews in Immunology 02/2003; 23(5-6):403-19. · 3.38 Impact Factor
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    ABSTRACT: Neoplastic transformation of cells is accompanied by an aberration of cell surface glycolipid composition. These tumor-associated, altered glycosphingolipids are often shed into the tumor cell microenvironment and mediate immunosuppressive activity. The nature and form of glycolipids shed by a variety of tumor cell lines and the mechanism(s) of shedding have been well characterized. The murine T cell lymphoma line, L5178Y-R, is known to shed a tumor-associated glycolipid, gangliotriaosylceramide, into the culture medium. We analyzed the effect of glycolipids from L5178Y-R on antigen presentation by murine CD1d1 molecules. CD1d1 molecules present glycolipid antigens to a specialized class of T cells called natural killer T (NKT) cells that mainly express a T cell receptor alpha chain (Valpha14Jalpha281) associated with Vbeta chains of limited diversity. In the current report, we found that L5178Y-R cells express CD1 on their cell surface yet are unable to stimulate CD1d1-specific NKT cells. We hypothesized that the glycolipid(s) shed by L5178Y-R inhibited antigen presentation by CD1d1. Pretreatment of CD1d1(+) cells with conditioned medium from L5178Y-R inhibited CD1-specific stimulation of canonical (Valpha14(+)) but not noncanonical (Valpha5(+)) NKT cells. Exogenous addition of lipids extracted from L5178Y-R cells as well as purified gangliotriaosylceramide mimicked this effect. Inhibition of glycolipid shedding in L5178Y-R cells with d-1-phenyl-2-hexadecanoylamino-3-morpholino-1-propanol resulted in the rescue of CD1d1 recognition by canonical (but not noncanonical) NKT cells. These results suggest that one means by which certain tumor cells can evade the host's innate antitumor immune response is by shedding glycolipids that inhibit CD1-mediated antigen presentation to NKT cells.
    Proceedings of the National Academy of Sciences 07/2002; 99(12):8197-202. · 9.81 Impact Factor

Publication Stats

214 Citations
34.36 Total Impact Points

Institutions

  • 2002–2010
    • Indiana University-Purdue University Indianapolis
      • Department of Microbiology and Immunology
      Indianapolis, IN, United States
  • 2005
    • Indiana University-Purdue University School of Medicine
      • Microbiology and Immunology
      Indianapolis, IN, United States