• YAKHAK HOEJI
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• v.50 no.4
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• pp.244-253
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• 2006

Effects of chrysene on immune functions were studied in female BALB/c mice. When mice were treated po with chrysene for 7 consecutive days, the antibody response was suppressed dose-dependently. Chrysene induced the enzyme activities of CYP LA and 2B time- and dose-dependently. In ex vivo lymphocyte proliferation, chrysene inhibited splenocyte proliferation by LPS and Con A. Moreover, the numbers of $CD4^+IL-2^+$ cells were reduced by chrysene. In conclusion, chrysene-induced immunotoxicity might be mediated, at least in part, via IL-2 production, and caused by mechanisms associated with metabolic activation.

• Animal cells and systems
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• v.4 no.4
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• pp.381-388
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• 2000

Using a murine T cell hybridoma, activation-induced cell death (AICD) was studied. As an in vitro model system for the AICD, 1 cell hybridoma expressing TCR/CD3 complex was incubated onto the immobilized purified anti-CD3 antibody. The immobilized anti-CD3 antibody induced AICD effectively up to 40%. At 1-100 $\mu$M range of SNP, an exogenous source of nitric oxide (NO), the cell proliferation was not affected, but at 1 mM SNP, cell proliferation was significantly reduced. The AICD of T cell hybridoma was inhibited by exogenous NO at non-cytotoxic concentration, In the cells undergoing AICD, the expressions of caspase-3 and FasL were detected, but not iNOS. Similar result was recognized in the apoptosis induced by dexamethasone, an apoptosis-inducing agent. However, the conversion from the inactive form of caspase-3 (32 kDa) to the active form (17 kDa) was significantly reduced in the cells in AICD induced by anti-CD3 antibody, With the result of increased PARP cleavage in the cells, we propose that another PARP cleavage pathway not involving caspase-3 may function in the anti-CD3 antibody induced AICD in the T cell hybridoma.

• Journal of Ginseng Research
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• v.27 no.3
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• pp.115-119
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• 2003

There has been continuing interest in the development of synthetic and natural compounds that modify the immune response particularly for the treatment of AIDS and cancer. During the past fifty years, numerous scientific studies have been published on ginseng. Modem human studies have investigated preventive effect of ginseng on several kinds of cancer, its long term immunological effect on HIV patients, its effect on cell mediated immune functions in healthy volunteers. Similarly non clinical studies on animal model system have studied the chemopreventive action of ginseng on cancer and immunological properties of ginseng. The precise mechanism of action of ginseng, however, not clearly understood. Considering its wide-ranging therapeutic effects, this study is being undertaken to elucidate the general mode of action of ginseng, especially to test our hypothesis that its biological action may be mediated by the immune system.

• Korean Journal of Veterinary Service
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• v.18 no.2
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• pp.182-188
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• 1995

Hemodynamic values were assessed in cows with naturally mastatis. hemodynamic tests included WBC, RBC, PCV, Hemoglobin, Monocyte, Eosinophil, Neutrophil, Lymphocyte, and prothrombin time, activated partial thromboplastin time, thrombin time, fibrinogen, platelet, antithrombin-III, and plasminogen activities. Significant changes were observed in the mean values of most analytses : WBC, monocytes, eosinophil, neutrophil were increased and Iymphocyte were decreased. prothrombin time was increased： activated partial thromboplastin time, thrombin time. increased : activated partial thromboplastin time, thrombin time, fibrinogen concentration, plasminogen activity and platelet concentration were decreased : and RBC, PCV, hemoglobin and antithrombin-III activity were unchanged, compared with normal mean values. Thesse data indicated activation of hemodynamic mechanisms, initiated either directly by bacteria produced endotoxin of secondaly inflammatory mediators produced in response to caused bacteria and naturally acquired mastitis was very similar to the experimental endotoxin-induced mastitis.

• Proceedings of the Korea Crystallographic Association Conference
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• 2003.05a
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• pp.13-13
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• 2003

B-cell activating factor (BAFF) is a key regulator of B-lymphocyte development. Its biological role is mediated by the specific receptors BCMA, TACI, and BAFF-R. We have determined the crystal structure of BAFF-R extracellular domain bound to BAFF at a resolution of 3.3 ?. The cysteine-rich domain(CRD) of the BAFF-R extracellular domain adopts a b-hairpin structure and binds to the virus-like BAFF cage in a 1:1 molar ratio. The conserved DxL motif of BAFF-R is located on the tip of the b-turn, and plays an indispensable role in the binding of BAFF. The crystal structure shows that a unique dimeric contact occurs between the BAFF-R monomers in the virus-like cage complex. Both of the CRDs of TACI contain the DxL motifs and simultaneously interact with the BAFF dimer in the virus-like cage.

• Molecules and Cells
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• v.22 no.3
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• pp.308-313
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• 2006

Stromal cell-derived factor (SDF-1) is a CXC chemokine that selectively activates the CXCR4 chemokine receptor. Fibronectin is an intracellular matrix component that binds integrin and mediates cell-matrix adhesion. Activation of the integrin receptor can occur in two ways: by ligand binding (outside-in signaling), and in response to intracellular events (inside-out signaling). In the current study we showed that SDF-$1{\alpha}$ inhibited adhesion of T lymphocyte Jurkat cells resulting from binding high concentrations of fibronectin as well as that of THP-1 monocytes. The effect of SDF-$1{\alpha}$ on fibronectin-mediated adhesion was partly reversed by the CXCR4 receptor antagonist T140. Our results suggest that an SDF-1/CXCR4 signal pathway modulates fibronectin-mediated lymphocytes adhesion.

• Journal of Medicine and Life Science
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• v.15 no.1
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• pp.1-5
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• 2018

Allergy is conditions when a hypersensitivity reaction happens with a certain element, called as an allergen, which is commonly not reactive to ordinary individuals. Allergic diseases involve various organs or systems in the body. The purpose of allergy tests is to make a diagnosis of allergic diseases and to identify the affecting allergens. In vivo tests, more relevant in clinical situation, include skin test, patch test and provocation test. In in vitro tests, there are specific IgE test, histamine releasing assay, and lymphocyte activation test, safer and more objective than in vivo tests. In the view point of clinical practice, skin test, provocation test, total IgE test and specific IgE test were reviewed in depth.

• The Korea Journal of Herbology
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• v.23 no.2
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• pp.99-109
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• 2008

Objectives : The present study was to investigate the effect of extract of Chelidonii herba (ECH) on the proliferation and activation of eosinophils which were prepared from lung cells of asthma-induced mouse by ovalbumin (OVA) treatment. Methods : C57BL/6 mouse was exposed to OVA three times a week for 6 weeks. The mouse lung tissues were dissected out, chopped and dossiciated with collagenase (1 ${\mu}g$/ml). Eosinophils were activated by rIL-3/rmIL-5 co-treatments. The lung cells were treated with ECH, incubated for 48 hr at $37^{\circ}C$, and analyzed by flow cytometery, ELISA, RT-PCR, and immuno-histochemical analysis. Results : In FACS analysis, number of granulocyte/lymphocyte, $CD3e^-$/$CCR3^+$, $CD3e^+$/$CD69^+$, $CD4^+$ and $CD23^+$/$B220^+$ in asthma-induced lung cells were significantly decreased by ECH treatment compared to the control group. And mRNA expression for IL-4, IL-5, IL-13, CCR3 and eotaxin in asthma-induced lung cells, which was induced by rIL-3 plus rmIL-5 treatments, was significantly decreased by ECH treatment. In ELISA analysis, production levels of IL-3, IL-5, IL-13 and histamine in asthma-induced lung cells, which were induced by rIL-3 plus rmIL-5 co-treatment, were significantly decreased by ECH treatment. ECH treatments significantly inhibited the proliferation of eosinohils prepared from asthma-induced mouse lung tissues compared to the non-ECH treated control cells. Immunohistochemical analysis revealed that ECH treatment significantly decreased the levels of eosipnphil activation compared to non-treated cells. Conclusions : The present data suggested that Chelidonium majus L. may have an effect on the inhibition of parameters associated with asthma responses in eosinpophils, and thus implicate the possibility for the clinical application of Chelidonium majus L.

• Archives of Pharmacal Research
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• v.22 no.4
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• pp.340-347
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• 1999

Dendritic cells (DCs) are potent professional antigen-presenting cells (APC) capable of inducing the primary T cell response to antigen. Although tumor cells express target antigens, they are incapable of stimulating a tumor-specific immune response due to a defect in the costimulatory signal that is required for optimal activation of T cells. In this work, we describe a new approach using tumor-DC coculture to improve the antigen presenting capacity of tumor cells which does not require a source of tumor-associated antigen. Immunization of a weakly immunogenic and progressive tumor cocultured with none marrow-derived DCs generated an effective tumor vaccine. Immunization with the cocutured DCs was able to induce complete protectiv immunity against tumor challenges and was effective for the induction of tumor-specific CTL (cytotoxic T lymphocyte) activity. Furthermore, high NK cell activity was observed in mice in which tumors were rejected. In addition, immunization with tumor-pulsed DC s induced delayed tumor growth, but not tumor eradication in tumor-bearing mice. Our results demonstrate that coculture of DCs with tumors generated antitumor immunity due to the NK cell activation as well as tumor-specific T cell. This approach would be used for designing tumor vaccines using DCs when the information about tumor antigens is limited.

• Molecules and Cells
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• v.43 no.11
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• pp.921-934
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• 2020

Lck-interacting transmembrane adaptor 1 (LIME) has been previously identified as a raft-associated transmembrane protein expressed predominantly in T and B lymphocytes. Although LIME is shown to transduce the immunoreceptor signaling and immunological synapse formation via its tyrosine phosphorylation by Lck, a Src-family kinase, the in vivo function of LIME has remained elusive in the previous studies. Here we report that LIME is preferentially expressed in effector T cells and mediates chemokine-mediated T cell migration. Interestingly, in LIME^-/- mice, while T cell receptor stimulation-dependent proliferation, differentiation to effector T cells, cytotoxic T lymphocyte (CTL) function and regulatory T lymphocyte (Treg) function were normal, only T cell-mediated inflammatory response was significantly defective. The reduced inflammation was accompanied by the impaired infiltration of leukocytes and T cells to the inflammatory sites of LIME^-/- mice. More specifically, the absence of LIME in effector T cells resulted in the reduced migration and defective morphological polarization in response to inflammatory chemokines such as CCL5 and CXCL10. Consistently, LIME^-/- effector T cells were found to be defective in chemokine-mediated activation of Rac1 and Rap1, and dysregulated phosphorylation of Pyk2 and Cas. Taken together, the present findings show that LIME is a critical regulator of inflammatory chemokine-mediated signaling and the subsequent migration of effector T cells to inflammatory sites.