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Chang, Jae-Hoon,Lee, Jung-Mi,Youn, Hyun-Jun,Lee, Kyoo-A,Chung, Yeonseok,Lee, Ah-Young,Kweon, Mi-Na,Kim, Ho-Youn,Taniguchi, Masaru,Kang, Chang-Yuil WILEY-VCH Verlag 2008 European journal of immunology Vol.38 No.10
<P>We previously showed that although systemic administration of α-galactosylceramide (αGalCer) or agonistic anti-CD40 induced functional maturation of dendritic cells (DC) in mesenteric lymph nodes, only the former treatment succeeded in breaking the induction of oral tolerance. In this study, we looked for the essential factor responsible for the disruption of oral tolerance. We found that lamina propria (LP)-DC was responsible for the oral OVA presentation and that Peyer's patch was not essential for the induction of oral tolerance. Therefore, we investigated the role of LP-DC. Treatment with αGalCer but not with anti-CD40 induced the full maturation of LP-DC at an early time point. This functional activation of LP-DC was mediated by strong activation of NKT cells that reside abundantly in the small intestinal lamina propria (SI-LP) and interferon-γ partially contributed to the LP-DC activation. LP-DC isolated from αGalCer-treated OVA-fed mice induced the differentiation of naïve CD4<SUP>+</SUP> T cells into Th1 and Th2 and was associated with the reduced Foxp3<SUP>+</SUP> population. In contrast, LP-DC isolated from anti-CD40-treated OVA-fed mice failed to generate Th cell differentiation but induced more Foxp3<SUP>+</SUP> CD4<SUP>+</SUP> T cells. Our results demonstrate that triggered by NKT cells in SI-LP, functional maturation of Ag-capturing DC from SI-LP is necessary for the abrogation of oral tolerance induction.</P>
Chang, Sun-Young,Ko, Hyun-Jeong,Heo, Tae-Hwe,Kang, Chang-Yuil American Society for Pharmacology and Experimental 2005 Molecular pharmacology Vol.67 No.5
<P>Endothelial monocyte-activating polypeptide-II (EMAP II) is an antiangiogenic factor for rapidly growing endothelial cells that is released from tumor cells under physiological stress such as hypoxia. We have previously shown that the interaction between EMAP II and the alpha-subunit of ATP synthase, alpha-ATP synthase, can play a regulatory function in the growth of endothelial cells. In the current study, we found that EMAP II-alpha-ATP synthase interaction could be inhibited by excess heparin, whereas the interaction could be enhanced by a low concentration of heparin. Both EMAP II and alpha-ATP synthase could specifically interact with heparin, and this interaction was increased under acidic conditions. In addition, EMAP II and alpha-ATP synthase were found to contain the heparin binding motifs determined by analysis using site-directed mutant forms. In endothelial cells, binding of EMAP II to cells was dramatically enhanced, and alpha-ATP synthase could associate with heparan sulfate at acidic pH. The inhibitory effect of EMAP II on the growth of cultured endothelial cells was also significantly enhanced at acidic pH. Analysis using mutant EMAP II proteins demonstrated that heparan sulfate was essential for the enhanced binding and EMAP II function to endothelial cells at acidic pH. Furthermore, the enhanced inhibitory effects of EMAP II could be abrogated by excess heparin or heparinase treatment. In the endothelial cell, heparan sulfate may regulate the function of EMAP II released from the tumor cell in hypoxic condition.</P>
Chang, Jae‐,Hoon,Kim, Yeon‐,Jeong,Han, Seung‐,Hee,Kang, Chang‐,Yuil WILEY‐VCH Verlag 2009 European journal of immunology Vol.39 No.5
<P><B>Abstract</B></P><P>Regulatory CD4<SUP>+</SUP> T cells are important for the homeostasis of immune cells, and their absence correlates with autoimmune disorders. However, how the immune system regulates Treg homeostasis remains unclear. We found that IFN‐γ‐deficient‐mice had more forkhead box P3 (FOXP3<SUP>+</SUP>) cells than WT mice in all secondary lymphoid organs except the thymus. However, T‐bet‐ or IL‐4Rα‐deficient mice did not show a similar increase. <I>In vitro</I> differentiation studies showed that conversion of naïve T cells into FOXP3<SUP>+</SUP> cells (neo‐generated inducible Treg (iTreg)) by TGF‐β was significantly inhibited by IFN‐γ in a STAT‐1‐dependent manner. Moreover, an <I>in vivo</I> adoptive transfer study showed that inhibition of FOXP3<SUP>+</SUP> iTreg generation by IFN‐γ was a T‐cell autocrine effect. This inhibitory effect of IFN‐γ on iTreg generation was significantly abrogated after <I>N</I>‐acetyl‐<SMALL>L</SMALL>‐cysteine treatment both <I>in vitro</I> and <I>in vivo</I>, indicating that IFN‐γ regulation of iTreg generation is dependent on ROS‐mediated apoptosis. Therefore, our results suggest that autocrine IFN‐γ can negatively regulate the neo‐generation of FOXP3<SUP>+</SUP> iTreg through ROS‐mediated apoptosis in the periphery.</P>
Chang Yuil Kang,Mi Ja Shim,Eung Chil Choi,Young Nam Lee,Byong Kak Kim ) 생화학분자생물학회 1981 BMB Reports Vol.14 No.2
To find antineoplastic components in Korean higher fungi, protein-bound polysaccharides were isolated from the carpophores of Laetiporus sulphureus and the mycelium of Ganoderma lucidum grown in shake culture. These compounds suppressed tumor growth of sarcoma 180 grafted in A-strain mice. These compounds were administered intraperitoneally to the mice at a dose of 50 ㎎/㎏ daily for five days. Ten days later the mice were immunized with 1×10^7 sheep red blood cells. The number of plaque-forming cells in their spleen was significantly greater than those of control mice. Three monosaccharides and fifteen amino acids were identified in the protein-bound polysaccharide of Laetiporus sulphureus. Three monosaccharides and sixteen amino acids were identified in that of Ganoderma lucidum.
Kang, Chang Yuil 가톨릭 의과학연구원 2001 가톨릭 의과학연구원 국제학술대회 Vol.5 No.-
4-1BB(CDw137) is a member of the tumor necrosis factor receptor superfamily and is expressed on activated T cells, monocytes, natural killer cells. The interaction of 4-1BB and 4-1BB ligand providers a costimulatory signal leading to T cell activation and growth. The expression of 4-1BB has been known to be a activation-dependent.
An antitumor component of laetiporus sulphureus and its immunostimulating activity
Kang, Chang-Yuil,Lee, Chong-Ock,Chung, Kyeong-Soo,Choi, Eung-Chil,Kim, Byong-Kak The Pharmaceutical Society of Korea 1982 Archives of Pharmacal Research Vol.5 No.2
A protein-polysaccharide fraction was prepared from the carpophores of Laetiporus sulphureus. This fraction suppressed growth of sarcoma 180 in A-strain mice when administered i. p. To investigate the mechanism of antitumor action of this fraction, plaque assay was conducted by administrating i. p. to the mise at a dose level of 50mg/kg for five days. Ten days later, the mice were immunized with 1 * 10$^{7}$ sheep red blooc cells. The number of hemolytic plaque forming cells was significantly greater than that of the control mice. Three monosaccharides and fifteen amino acids were identified in the protein-polysaccharide fraction.
Kim, Yun-Sun,Kim, Yeon-Jeong,Lee, Jung-Mi,Kim, Eun-Kyung,Park, Young-Jun,Choe, Su-Kyong,Ko, Hyun-Jeong,Kang, Chang-Yuil Williams Wilkins 2012 JOURNAL OF IMMUNOLOGY Vol.188 No.9
<P>Myeloid-derived suppressor cells (MDSCs) are increased by tumor-derived factors and suppress anti-tumor immunity. MDSCs obtained at a late time point after tumor injection had stronger suppressive activity than MDSCs obtained at an early time point, as measured by T cell proliferation assays. To find factors in MDSCs that change during tumor growth, we analyzed gene expression profiles from MDSCs at different time points after tumor injection. We found that immune response-related genes were downregulated but protumor function-related genes were upregulated in both monocytic MDSCs (Mo-MDSCs) and polymorphonuclear granulocytic MDSCs (PMN-MDSCs) at the late time point. Among differentially expressed genes, FK506 binding protein 51 (FKBP51), which is a member of the immunophilin protein family and plays a role in immunoregulation, was increased in the Mo-MDSCs and PMN-MDSCs isolated from the late time points. Experiments using small interfering RNA and a chemical inhibitor of FKBP51 revealed that FKBP51 contributes to the regulation of the suppressive function of MDSCs by increasing inducible NO synthase, arginase-1, and reactive oxygen species levels and enhancing NF-κB activity. Collectively, our data suggest that FKBP51 is a novel molecule that can be targeted to regulate the immunosuppressive function of MDSCs.</P>
Chung, Yeonseok,Chang, Jae-Hoon,Kim, Byung-Seok,Lee, Jung-Mi,Kim, Ho-Youn,Kang, Chang-Yuil VCH Verlagsgesellschaft mbH, etc 2007 European journal of immunology Vol. No.
<P>In the spleen, exogenous antigen is preferentially presented by CD8&agr;<SUP>+</SUP>CD11b<SUP>–</SUP> DC to CD8 T cells and by CD8&agr;<SUP>–</SUP>CD11b<SUP>+</SUP> DC to CD4 T cells. However, it is not yet clear whether the same rule applies to other secondary lymphoid organs. To address this issue, we first classified secondary lymphoid tissues into three categories based on the expression pattern of CD8&agr; and CD11b in C57BL/6 and BALB/c mice: (a) spleen, (b) mesenteric lymph node (MLN) and (c) other peripheral lymph nodes (PLN). We then analyzed the OVA-specific T cell-stimulating capacity of each DC subset after intravenous injection with soluble OVA. Our results show that, regardless of tissue origin, CD8&agr;<SUP>–</SUP>CD11b<SUP>+</SUP> DC generally present OVA to CD4 T cells, a finding that held true as well for CD8&agr;<SUP>+</SUP>CD11b<SUP>+</SUP> DC in PLN. In striking contrast, CD8&agr;<SUP>+</SUP>CD11b<SUP>–</SUP> DC in spleen, CD8&agr;<SUP>–</SUP>CD11b<SUP>+</SUP> DC in MLN and CD8&agr;<SUP>+</SUP>CD11b<SUP>+</SUP> DC in PLN mainly cross-present OVA to CD8 T cells in their respective tissues. Of note, CD8&agr;<SUP>–</SUP>CD11b<SUP>+</SUP> DC in MLN and CD8&agr;<SUP>+</SUP>CD11b<SUP>+</SUP> DC in PLN present OVA to both CD4 T and CD8 T cells. Therefore, the antigen-presenting capacity of each distinct DC subset is determined by its anatomic environment in combination with its surface phenotype.</P>