• Korean Journal of Veterinary Pathology
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• v.1 no.1
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• pp.7-12
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• 1997

Lethally irradited C3H/HeN mice were transplanted with syngeneic bone marrow. The B cell regeneration levels of spontaneous serum Ig, fecal igA and specific ig to diphtheria toxoid were determined at various time points. The number of B220+ cells reached normal range at 4 weeks after bone marrow transplantation(BMT) in spleen and lymph node. The B cell number of spleen returned to normal relatively soon than in the lymph node. Within 5 to 7 weeks after BMT, the transplanted mice contained nearly normal levels of spontaneous serum IgA, IgG2b and fecal IgA, but 2 fold lower levels of serum IgG2a, IgM and IgG3. Especially IgG3 levels were within low-normal range throughout the study. One to two weeks after immunization the predominant anti-diphtheria toxoid subtype was IgM. The levels of specific serum Ig were very low and after booster immunization at week 6, the short-lasting increase of Ig production was notd.

• Journal of Microbiology and Biotechnology
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• v.14 no.1
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• pp.167-170
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• 2004

Lactic acid bacteria (LABs) have been proposed as a potential oral allergy-therapeutic means of modulating immune phenotype expression in vivo, via promoting or reducing cytokine production. This study investigated the ability of LABs to suppress allergic response via modulating cytokine production in mice splenocytes. BALB/c mice were intraperitoneally primed with ovalbumin together with alum adjuvant to invoke antigen-specific Th1/Th2 cytokine-secreting cell populations in splenocytes. Spleen cells from mice fed with Lactobacillus confusus PL9001 (KCCM-10245), L. fermentum PL9005 (KCCM-10250), L. plantarum PL9011 (KCCM-10358), and Bifidobacterium infantis PL9506 (KCCM-10406) suppressed the levels of Th2 cell cytokines such as IL-4 and IL-5 during antigen sensitization. In addition, all mice fed with LABs induced secretion of Th1 cell cytokines such as IL-2 in splenocytes. These results suggested that LABs are anti-allergic agents, in view of their Th1/anti-Th2 immunoregulation.

• Development and Reproduction
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• v.13 no.3
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• pp.145-153
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• 2009

Previously, we obtained the list of genes differentially expressed between GV and MII oocytes. Out of the list, we focused on functional analysis of Zap70 in the present study, because it has been known to be expressed only in immune cells. This is the first report about the expression and its function of Zap70 in the oocytes. Synthetic 475 bp Zap70 dsRNA was microinjected into the GV oocytes, and the oocytes were cultured in vitro. In addition to maturation rates, meiotic spindle and chromosome rearrangements, and changes in expression levels of transcripts of three kinases, Erk1/2, JNK, and p38, were determined. Zap70 is highly expressed in immature GV oocytes, and gradually decreased as oocyte matured. When dsRNA of Zap70 was injected into the GV oocytes, Zap70 mRNA specifically and completely decreased by 2 hr and its protein expression also decreased significantly. Absence of Zap70 resulted in maturation inhibition at meiosis I (57%) with abnormalities in meiotic spindle formation and chromosome rearrangement. Concurrently, mRNA expression of Erk2, JNK, and p38, were affected by Zap70 RNAi. Therefore, we concluded that Zap70 is involved in MI-MII transition by affecting expression of MAP kinases.

• The Korea Journal of Herbology
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• v.26 no.4
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• pp.83-88
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• 2011

Objectives : The aim of this study was to investigate the asthma-suppressive and immuno-regulatory effect of Notopterygii Rhizoma(NR) extract on OVA(ovalbumin)-induced asthma in mice. Methods : C57BL/6 mice out of all the experimental groups, except the Normal group and the NRI group, were sensitized and challenged with OVA. C57BL/6 mice were exposed to OVA three times a week for 12 weeks and analyzed by flow cytometer, ELISA, H&E stain. Results : The concentrations of IL-4, IL-5, IL-13, IgE in serum of the OVA-NRII group decreased significantly compared with those of the OVA-Control group. The number of $Gr-1^+/CD11b^+$, $CCR3^+$, $CD3^+/CD19^+$, $CD3e^+/CD69^+$cells in the OVA-NRI group decreased significantly compared with those of the OVA-Control group. The collagen accumulation in the lung sections of the OVA-NRII group decredased signi- ficantly compared with that of the OVA-Control group. Conclusions : These results suggest that Notopterygii Rhizoma(NR) would be a effective candidate for herbal-originated anti-asthmatic drug. However, this drug should be further studied for characterization of the accurate action and underlying mechanism using variant disease model in the future.

• Journal of Ginseng Research
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• v.42 no.4
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• pp.476-484
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• 2018

Background: Korean Red Ginseng (steamed and dried white ginseng, Panax ginseng Meyer) is well known for enhancing vital energy and immune capacity and for inhibiting cancer cell growth. Some clinical studies also demonstrated a therapeutic potential of ginseng extract for treating lung inflammatory disorders. This study was conducted to establish the therapeutic potential of ginseng saponins on the lung inflammatory response. Methods: From Korean Red Ginseng, 11 ginsenosides (Rb1, Rb2, Rb3, Rc, Rd, Re, Rf, Rg1, Rg2, Rg3, and Rh2) were isolated. Their inhibitory potential and action mechanism were evaluated using a mouse model of lung inflammation, acute lung injury induced by intranasal lipopolysaccharide administration. Their anti-inflammatory activities were also examined in lung epithelial cell line (A549) and alveolar macrophage (MH-S). Results: All ginsenosides orally administered at 20 mg/kg showed 11.5-51.6% reduction of total cell numbers in bronchoalveolar lavage fluid (BALF). Among the ginsenosides, Rc, Re, Rg1, and Rh2 exhibited significant inhibitory action by reducing total cell numbers in the BALF by 34.1-51.6% (n = 5). Particularly, Re showed strong and comparable inhibitory potency with that of dexamethasone, as judged by the number of infiltrated cells and histological observations. Re treatment clearly inhibited the activation of mitogen-activated protein kinases, nuclear factor-${\kappa}B$, and the c-Fos component in the lung tissue (n = 3). Conclusion: Certain ginsenosides inhibit lung inflammatory responses by interrupting these signaling molecules and they are potential therapeutics for inflammatory lung diseases.

• IMMUNE NETWORK
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• v.11 no.2
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• pp.100-106
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• 2011

Background: Disparities of Minor H antigens can induce graft rejection after MHC-matched transplantation. H60 has been characterized as a dominant antigen expressed on hematopoietic cells and considered to be an ideal model antigen for study on graft-versus-leukemia effect. Methods: Splenocytes from C57BL/6 mice immunized with H60 congenic splenocytes were used for establishment of H60-specific CTL clones. Then the clones were characterized for proliferation capacity and cytotoxicity after stimulation with H60. Clone #14, #15, and #23 were tested for the TCR binding avidity to H60-peptide/$H-2K^b$ and analyzed for TCR sequences. Results: H60-specific CTL clones showed different levels of proliferation capacity and cytotoxic activity to H60-stimulation. Clones #14, #15, and #23 showed high proliferation activity, high cytotoxicity, and low activities on both aspects, respectively, and have TCRs with different binding avidities to H60-peptide/$H-2K^b$ with $t_{1/2}$ values of 4.87, 6.92, and 13.03 minutes, respectively. The TCR usages were $V{\alpha}12D-3-01+J{\alpha}11-01$ and $V{\beta}12-1-01+D{\beta}1-01+J2-7-01$ for clone #14, $V{\alpha}13D-1-02+J{\alpha}34-02$ and $V{\beta}13-1-02+D{\beta}2-01+J{\beta}2-7-01$ for clone #15, and $V{\alpha}16D+J{\alpha}45-01$ and $V{\beta}12-1-01+D{\beta}1-01+J{\beta}2-5-01$ for clone #23. Conclusion: The results will be useful for modeling GVL and generation TCR transgenic mouse.

• BMB Reports
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• v.33 no.6
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• pp.463-468
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• 2000

Anthrax lethal toxin, which consists of two separate protein, protective antigen (83 KDa) and lethal factor (85 KDa) is responsible for major symptoms and death from systemic infection of Bacillus anthracis. High concentrations of this toxin are cytolytic to macrophages, whereas sublytic concentrations of lethal toxin induce these cells to produce interleukin $1{\beta}$ ($IL-1{\beta}$). It is proposed that melatonin and dehydroepiandrosterone (DHEA) may play an important role in modifying immune dysfunction. In this study, we investigated whether or not melatonin and DHEA could prevent $IL-1{\beta}$ production that is induced by anthrax lethal toxin in mouse peritoneal macrophages. Treatment of melatonin or DHEA alone, as well as together, prevented the production of $IL-1{\beta}$ caused by anthrax lethal toxin. We found that melatonin at a concentration of $10^{-6}-10^{-7}$ M inhibits $IL-1{\beta}$ production induced by anthrax lethal toxin. As expect, treatment of DHEA at a concentration $10^{-6}-10^{-7}$ M also suppressed production of $IL-1{\beta}$ by lethal toxin stimulated macrophages. The results of these studies suggest that melatonin and DHEA, immunomodulators, may have an important role in reducing the increase of cytokine production in anthrax lethal toxin-treated macrophages.

• BMB Reports
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• v.47 no.7
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• pp.399-404
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• 2014

B7-H4 is a member of B7 family of co-inhibitory molecules and B7-H4 protein is found to be overexpressed in many human cancers and which is usually associated with poor survival. In this study, we developed a therapeutic vaccine made from a fusion protein composed of a tetanus toxoid (TT) T-helper cell epitope and human B7-H4IgV domain (TT-rhB7-H4IgV). We investigated the anti-tumor effect of the TT-rhB7-H4IgV vaccine in BALB/c mice and SP2/0 myeloma growth was significantly suppressed in mice. The TT-rhB7-H4IgV vaccine induced high-titer specific antibodies in mice. Further, the antibodies induced by TT-rhB7-H4IgV vaccine were capable of depleting SP2/0 cells through complement-dependent cytotoxicity (CDC) in vitro. On the other hand, the poor cellular immune response was irrelevant to the therapeutic efficacy. These results indicate that the recombinant TT-rhB7-H4IgV vaccine might be a useful candidate of immunotherapy for the treatment of some tumors associated with abnormal expression of B7-H4.

• Molecules and Cells
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• v.38 no.1
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• pp.26-32
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• 2015

Toll-like receptors (TLR) 7 and 9 transduce a cellular signal through the MyD88-dependent pathway and induce the production of inflammatory mediators against microbial nucleotide components. The repeated stimulation of TLR4 leads to endotoxin tolerance, but the molecular mechanisms of tolerance induced through the costimulation of individual TLR has not yet been established, although endosomal TLRs share signaling pathways with TLR4. In the present study, mouse macrophages were simultaneously stimulated with the TLR7 agonist, gardiquimod (GDQ), and the TLR9 agonist, CpG ODN 1826, to examine the mechanism and effector functions of macrophage tolerance. Compared with individual stimulation, the costimulation of both TLRs reduced the secretion of TNF-${\alpha}$ and IL-6 through the delayed activation of the NF-${\kappa}B$ pathway; notably, IL-10 remained unchanged in costimulated macrophages. This tolerance reflected the early induction of suppressor of cytokine signaling-1 (SOCS-1), according to the detection of elevated TNF-${\alpha}$ secretion and restored NF-${\kappa}B$ signaling in response to the siRNA-mediated abrogation of SOCS-1 signaling. In addition, the restimulation of each TLRs using the same ligand significantly reduced the expression of both TLRs in endosomes. These findings revealed that the costimulation of TLR7 and TLR9 induced macrophage tolerance via SOCS-1, and the restimulation of each receptor or both TLR7 and TLR9 downregulated TLR expression through a negative feedback mechanisms that protects the host from excessive inflammatory responses. Moreover, the insufficient and impaired immune response in chronic viral infection might also reflect the repeated and simultaneous stimulation of those endosomal TLRs.

• Korean Journal of Agricultural Science
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• v.49 no.1
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• pp.11-18
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• 2022

A disrupted immune system during pregnancy is involved in pregnancy complications, such as spontaneous abortion, preeclampsia, and recurrent pregnancy loss. This study examined the role of toll-like receptor (TLR) 4 and ASC (apoptosis-associated speck-like protein containing a CARD [c-terminal caspase recruitment domain]) in pregnancy complications using a lipopolysaccharide (LPS)-induced miscarriage mice model. Incidences of miscarriage and embryonic resorption were examined at 9.5 days of pregnancy in wild-type (WT), ASC knockout (KO), and TLR4 KO mice after injecting them with LPS. The fetuses and placenta were obtained after sacrifice at 15.5 days of pregnancy. A significantly lower frequency of fetus absorption was found in TLR4 KO mice, whereas corresponding absorption outcomes were strongly induced in the WT and ASC KO mice upon an LPS injection. As expected, TLR4 KO mice were resistant to LPS-induced abortion. A histological analysis of the miscarried placenta showed increasing levels of the eosin staining of spongiotrophoblast cells without any obvious difference between WT and ASC KO mice. These results suggest that TLR4 KO mice are resistant to LPS, which affects pregnancy persistence, whereas WT and ASC KO mice show high miscarriage rates due to LPS. Moreover, the ASC adaptor is not directly involved in LPS-induced miscarriages, and the NLRP3 inflammasome can be activated by other proteins in the absence of ASC.