• Journal of Pharmacopuncture
• /
• v.14 no.2
• /
• pp.15-24
• /
• 2011

Background: Type I allergy is involved in allergic asthma, allergic rhinitis, and atopic dermatitis which are accompanied by an acute and chronic allergic inflammatory responses. Rehmannia glutinosa is a traditional medicine in the East Asian region. This study examined whether a Rehmannia Glutinosa pharmacopuncture solution (RGPS) had anti-allergic or anti-inflammatory effects in antigen-stimulated-RBL-2H3 cells. Methods: We determined the effect of RGPS on cell viability using the 3-[4,5-dimethylthiazolyl]-2,5-diphenyltetrazolium bromide (MTT) assay. We also examined the effect of RGPS on the release of ${\beta}$-hexosaminidase and the secretion of IL-4 and TNF-${\alpha}$ using ELISA. In addition, we evaluated the effect of RGPS on the mRNA expression of various cytokines; IL-2, IL-3, IL-4, IL-5, IL-13 and TNF-${\alpha}$ using RT-PCR. Furthermore, we assessed the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-${\kappa}$B using Western blotting after RGPS treatment. Results: We found that RGPS ($10^{-4}$ to $10^{-1}$ dilution) did not cause any cytotoxicity. We observed significant inhibition of ${\beta}$-hexosaminidase release and suppression of the protein secretion of IL-4 and TNF-${\alpha}$ and mRNA expression of multiple cytokines in antigen-stimulated-RBL-2H3 cells after RGPS treatment. Additionally, RGPS suppressed not only the phosphorylation of MAPKs, but also the transcriptional activation of NF-${\kappa}$B in antigen-stimulated-RBL-2H3 cells. Conclusions: These results suggest that RGPS inhibits degranulation and expression of cytokines including IL-4 and TNF-${\alpha}$ via down-regulation of MAPKs and NF-${\kappa}$B activation in antigen-stimulated-RBL-2H3 cells. In conclusion, RGPS may have beneficial effects in the exerting anti-allergic or anti-inflammatory activities.

• Proceedings of the KSAR Conference
• /
• 2001.03a
• /
• pp.47-47
• /
• 2001

The neuropeptide vasopressin (VP) is a nine- amino acid hormone synthesized as preprohormone in the cell bodies of hypothalamic magnocellular neurons. The tumor in magnocellular neurons of the hypothalamus is associated with disfunctions of the cell bodies, leading to the diabetes insipidus. In order to study with the diabetes insipidus caused by a defect in VP synthesis and its secretion, we have produced the transgenic mice regulated by vasopressin promoter inserted to SV40 T antigen coding sequence (pVPSV.IGR2.1). One transgenic line expressing high levels of SV40 T antigen was propagated. The founder and all transgene positive adult animals have appeared with shorten mortality or apparent phenotypic abnormalities, including immune complex disease, and eventually die between 4 and 8 months of age. The mRNA and protein of SV40T antigen transgene were detected in brain of fetus as well as in brain, spleen, lung and lymph node in moribund at the age of 20 weeks. Histological analysis of transgenic mice showed that tumor developed in brain similar to primitive neuroectodermal tumors (PNET) in man. We also detected lymphomas in spleen and lymph node, and consequent tumor formation in various tissues of the transgenic mice. In pVPSV.IGR2.1, 21% mice showed brain tumor (PNET) at 5 weeks and 100% mice showed brain tumor after 15 weeks. In addition, Expression of apoptosis related genes (Bcl-28 & Bax) was increased over their age in mice with PNET as compared to control mice. Apoptosis related gene expression might be deregulated in mice with brain tumor. However, transgenic mice were not developed with the diabetes insipidus. These mice represent the first disease model to exhibit primitive neuroectodermal tumor in brain, as well as a unique model system for exploring the cellular pathogenesis of lymphomas.

• IMMUNE NETWORK
• /
• v.7 no.4
• /
• pp.173-178
• /
• 2007

Background: We studied the role for expression of CD40 and CD40L by CD4 and CD8 T cells in the generation of CD8 T cell response to minor histocompatibility antigen, H60. H60 is a cellular antigen to which CD8 responses require CD4 T cell help. Methods: CD40- or CD40L-deficient mice were adoptively transferred with normal CD4 or CD8 T cells or with memory CD4 or CD8 T cells, and were immunized with male H60 congenic splenocytes to induce CD8 T cell response to H60. Peripheral blood CD8 T cell from the immunized mice were stained with the H60 tetramer. Results: CD8 T cell response to H60 was not induced in both CD40- and CD40L-deficient mice. Adoptive transfer of $CD40^{+/+}$ CD8 T cells into CD40-deficient mice did not compensate the defect in inducing CD8 T cell response to H60, while the H60-specific CD8 T cells were activated in the CD40-deficient mice that were adoptively transferred with $CD40^{+/+}$ CD4 T cells. Adoptive transfer of $CD40L^{+/+}$ CD4 T cells into CD40L-deficient mice induced primary CD8 T cell response for H60 and the presence of $CD40L^{+/+}$ CD4 T cells was required even for memory CD8 T cells response to H60. Conclusion: Our results suggest that the CD40-CD40L interaction mediates the delivery of CD4 T cell help to naive and memory H60-specific CD8 T cells. While the expression of CD40L by CD4 T cells is essential, signaling through CD40 on CD8 T cells is not required for the induction of CD8 T cell response to H60.

• Biomolecules & Therapeutics
• /
• v.21 no.1
• /
• pp.35-41
• /
• 2013

Metformin is widely used for T2D therapy but its cellular mechanism of action is undefined. Recent studies on the mechanism of metformin in T2D have demonstrated involvement of the immune system. Current immunotherapies focus on the potential of immunomodulatory strategies for the treatment of T2D. In this study, we examined the effects of metformin on the antigen-presenting function of antigen-presenting cells (APCs). Metformin decreased both MHC class I and class II-restricted presentation of OVA and suppressed the expression of both MHC molecules and co-stimulatory factors such as CD54, CD80, and CD86 in DCs, but did not affect the phagocytic activity toward exogenous OVA. The class II-restricted OVA presentation-regulating activity of metformin was also confirmed using mice that had been injected with metformin followed by soluble OVA. These results provide an understanding of the mechanisms of the T cell response-regulating activity of metformin through the inhibition of MHC-restricted antigen presentation in relation to its actions on APCs.

• Proceedings of the Zoological Society Korea Conference
• /
• 1994.10a
• /
• pp.161.2-161
• /
• 1994

No Abstract, See Full Text

• 대한치주과학회:학술대회논문집
• /
• 2000.11a
• /
• pp.66-66
• /
• 2000

• Parasites, Hosts and Diseases
• /
• v.40 no.1
• /
• pp.59-64
• /
• 2002

A Cryptosporidium parvum sporozoite and oocyst λgt11 cDNA library was screened with a hyperimmune rabbit serum that was developed against insoluble fragments of ultrasonicated oocysts. A clone named Cp22.4.1 encoding a protein of 231 amino acids with 4 zinc-finger domains characterized by a Cys-X2-Cys-X4-His-X4-Cys motif was isolated and characterized. There was a complete match between the sequencing data of the coding region of Cp22.4.1 and the corresponding gene at chromosomal level. Cloning in a pBAD-TOPO-TA expression vector permitted to evaluate the antigenicty of the recombinant His-tagged antigen. This antigen was recognized by 2 out of 5 sera from Cruptosporidium immune calves and not by sera from parasite naive animals.

• Korean Journal of Microbiology
• /
• v.54 no.3
• /
• pp.222-227
• /
• 2018

Mycobacterium tuberculosis (MTB)-originated lipid antigen is presented on the antigen-presenting cell surface with CD1b. When monocyte-derived dendritic cells phagocytosed MTB H37Rv (Multiplicity of infection 10, infectivity: 46.89%), the CD1b expression level decreased slowly. Since this was just a live MTB-mediated phenomenon, it was not detected from heat-killed MTB or mycolic acid, which is a unique antigen of MTB. We confirmed that the phosphorylation of CD1b molecules using 2D electrophoresis with staining could phosphorylate and induce the presentation of the lipid antigen using the phagocytosis assay.

• IMMUNE NETWORK
• /
• v.7 no.2
• /
• pp.80-86
• /
• 2007

Background: CD40-activated B (CD40-B) cells might be an attractive source of autologous antigen-presenting cells (APCs) for immunotherapy due to the convenience to obtain from peripheral blood and expand in vitro. Moreover, CD40-B cells were found to be comparable with DCs in their capacity to raise antigen-specific CD8+ T cells. Here, we have established K562 cells expressing CD40L to expand CD40-activated B cells used for APCs. Methods: After activation of B cell by K562/CD40L, CD40-B cells were examined by counting B cell numbers. Surface expression of CD54, CD80, CD86 and HLA class II was measured by flow cytometry. The CD40-B cells were tested for its function as APC by mixed lymphocyte reactions (MLR) and by induction of T cell responses specific for pp65 peptide in vitro. Results: The expansion of B cells by K562/CD40L increased about 6-folds compared with anti-CD40 or K562. Furthermore, the expression of CD54, CD80, CD86 and HLA class II was up-regulated by K562/CD40L. B cells by K562/CD40L showed comparable antigen presentation activity with mature DCs as shown in MLR, INF-${\gamma}$ ELISPOT assay. Conclusion: These results suggest that K562/CD40L could be used to generate activated B cells as potent APCs which could be useful for cellular vaccination and adoptive immunotherapy.

• Biomolecules & Therapeutics
• /
• v.19 no.1
• /
• pp.77-83
• /
• 2011

Sulforaphane is an isothiocyanate found in cruciferous vegetables that has been reported to be an effective cancer preventive agent inducing growth arrest and/or cell death in cancer cells of various organs. This paper reports that sulforaphane exerts immunomodulatory activity on the MHC-restricted antigen presenting function. Sulforaphane efficiently increased the class II-restricted presentation of an exogenous antigen, ovalbumin (OVA), in both dendritic cells (DCs) and peritoneal macrophages in vitro. The class II-restricted OVA presentation-enhancing activity of sulforaphane was also confirmed using mice that had been injected with sulforaphane followed by soluble OVA. On the other hand, sulforaphane did not affect the class I-restricted presentation of exogenous OVA at concentrations that increase the class II-restricted antigen presentation. At a high concentration ($20\;{\mu}M$), sulforaphane inhibited the class I-restricted presentation of exogenous OVA. Sulforaphane did not affect the phagocytic activity of the DCs, and the cell surface expression of total H-$2K^b$, B7-1, B7-2 and CD54 molecules, even though it increased the expression of I-$A^b$ molecules to a barely discernable level. These results show that sulforaphane increases the class II-restricted antigen presenting function preferentially, and might provide a novel insight into the mechanisms of the anti-cancer effects of sulforaphane.