• Advances in Traditional Medicine
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• v.8 no.1
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• pp.1-16
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• 2008

Immunity is responsible for the defense mechanism of the body but in case of autoimmune diseases, its role gets diverted. Like so many other diseases, asthma is also considered as one of the most common autoimmune diseases to be occurring in community. Asthma is defined as a chronic inflammatory airway disease that is characterized by airway hyper reactivity and mucus hypersecretion that result in intermittent airway obstruction. The incidence of allergic asthma has almost doubled in the past two decades. Although, precise causative mechanism of asthma is unknown, but several mechanisms have been proposed that is immunological, pharmacological and genetic mechanisms, and airway and neurogenic inflammation. The inflammatory process observed in the asthmatic patients is the final result of a complex network of interactions between various immunological cell lineages, its mediators and secreted substances. Thus, among the mechanisms proposed, the immunological one plays a key role. Through this article, we have tried to provide some insight into immunological mechanisms in pathogenesis of asthma.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.1
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• pp.196-201
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• 2006

Electroacupuncture(EA) is commonly used in various diseases. In the present study, the effect of EA in the allergic mouse model was examined. Allergy is generated via immunological mechanism and non-immunological mechanism. Mast cells activated dy those mechanisms get to release various substances such as histamine, leukotrienes, prostaglandin, TNF-$\alpha$, IL-4, IL-6, etc. which induce allergic reactions and the following inflammatory responses. To evaluate the anti-allergic effects of EA, mortality, ear swelling response, vascular permeability and cytokine secretion were investigated in EA group and non-EA group of which mice were compound 48/80-induced allergy model or PCA model. Compound 48/80 induces allergic reaction via non-immunological mechanism and PCA model is generated through the same mechanism with immediate-type(Type1) allergic reaction, one of immunological allergic reactions. EA inhibited compound 48/80-induced ear swelling response but did not inhibit the systemic anaphylaxis. EA also inhibited passive cutaneous anaphylaxis(PCA) activated dy anti-dinitrophenol IgE. In addition, EA inhibited IL-6 and TNF-$\alpha$ secretion from 48 h PCA in mice. These results indicate that EA may be used for the treatment of mast cell-mediated allergic diseases, especially immediate-type(Type 1) allergy and non-immunologically mediated allergy.

• The Korean Journal of Pain
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• v.34 no.4
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• pp.463-470
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• 2021

Background: Although neuropathic pain is a severe and common pain, its pathophysiology has not been elucidated yet. Studies in recent years have focused on the immune system's role in the pathogenesis of neuropathic pain. The aim of this study was to investigate the role of immunological mechanisms in neuropathic pain and the effect of pregabalin by measuring immunological marker levels in peripheral blood before and after pregabalin treatment in postherpetic neuralgia (PHN) patients with neuropathic pain. Methods: Forty patients diagnosed with PHN were included in the study. CD4, T follicular cells (Tfh: CD4⁺CXCR5⁺PD1⁺), Th17 (CD4⁺CCR6⁺ and CD4⁺IL17A⁺), regulatory T cells (Treg: CD4⁺ CD25⁺foxp3⁺), Th1 (CD4⁺ CXCR3⁺ and CD4⁺ IFN-γ⁺) and Th2 (CD4⁺ IL-4⁺) cell ratios were measured in peripheral blood samples before treatment and after 3 months of treatment. Results: When immunological marker and inflammation parameter levels were compared before and after treatment, the helper T cell ratio (CD3⁺, CD4⁺) was 30.28 ± 12.27% before treatment and 34.93 ± 11.70% after treatment, so there was a statistically significant increase (P = 0.028). Th17 was 4.75 ± 5.02% before treatment and 5.80 ± 3.13% after treatment, and there was a statistically significant increase (P = 0.036). Conclusions: Immunological mechanisms play an essential role in the pathogenesis of neuropathic pain, immunologically based treatment approach will be the critical point of treatment.

• Journal of Haehwa Medicine
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• v.17 no.2
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• pp.69-86
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• 2008

In order to validate the objective efficacy of CBPT on anti-asthma and to develop effective therapeutics for asthma treatments, immunological modulatory mechanism was studied using animal model using OVA-Alum. The results are listed below. When treated with CBPT, survival rate of hFCs at 250 ug/ml was above 90%. AST and ALT, indicators of liver function measurements were in the normal range. Compared to the control group, CBPT treated group showed significant reduction in liver weights at both 400 and 200 mg/kg, and significant decrease of total liver cells at 400 mg/kg. Significant increase in CD4+ and CD8+ cells in DLN was observed in the CBPT treated group. Slight increase in CD3+, CD4+/CD25+ cells were also observed. On the other hand, CBPT significantly reduced the CD3+/CD69+ cell numbers at both concentrations. Slight decrease of CD19+ cells was also observed. CBPT significantly reduced the CD3e+/CD69+, CCR3+ and CD11b+/Gr-1+ cells in lung tissues at both doses. However, significant decrease of CD3e+ and B220+/IgE+ cells was only observed at 400 mg/kg dosed group. The results above strongly suggest the anti-asthmatic effect of CBPT through immunological modulation. By using various concentrations of CBPT, broader clinical applications of CBPT on anti-asthmatic treatment can be developed. The EBM database should provide valuable information in the development of drugs for asthma treatments.

• IMMUNE NETWORK
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• v.11 no.6
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• pp.383-389
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• 2011

Background: EY-6 is one of the newly synthesized indoledione derivatives to induce tumor cell-specific cell death. In this study, we investigated the mechanism of immunological death induced by EY-6 at mouse colon cancer cell as well as at the normal immune cell represented by dendritic cell. Methods: C57BL/6 mouse syngeneic colon cancer cell MC38 was treated with EY-6, and analyzed by MTT for viability test, flow cytometry for confirming surface expressing molecules and ELISA for detection of cytokine secretion. Normal myeloid-dendritic cell (DC) was ex vivo cultured from bone marrow hematopoietic stem cells of C57BL/6 mice with GM-CSF and IL-4 to analyze the DC uptake of dead tumor cells and to observe the effect of EY-6 on the normal DC. Results: EY-6 killed the MC38 tumor cells in a dose dependent manner (25, 50 and $100{\mu}M$) with carleticulin induction. And EY-6 induced the secretion of IFN-${\gamma}$ but not of TNF-${\alpha}$ from the MC38 tumor cells. EY-6 did not kill the ex-vivo cultured DCs at the dose killing tumor cells and did slightly but not significantly induced the DC maturation. The OVA-specific cross-presentation ability of DC was not induced by chemical treatment (both MHC II and MHC I-restricted antigen presentation). Conclusion: Data indicate that the EY-6 induced tumor cell specific and immunological cell death by modulation of tumor cell phenotype and cytokine secretion favoring induction of specific immunity eliminating tumor cells.

• BMB Reports
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• v.34 no.5
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• pp.408-414
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• 2001

Ornithine decarboxylase (EC 4.1.1.17) is an essential enzyme for polyamine synthesis and growth in mammalian cells and plants. We compared the biochemical and immunological properties of rat and Nicotiana glutinosa ODC by cloning and expressing the recombinant proteins. The primary amino acid sequence between rat and N. glutinosa ODC had a 40% homology The molecular weight of the overexpressed rat ODC was 53 kDa, and that of N. glutinosa was 46.5 kDa. Adding 1 mM of putrescine to the enzyme reaction mixture inhibited both rat and N. glutinosa ODC activity to 30%. Agmatine had an inhibitory effect only on N. glutinosa ODC. Cysteine and lysine modifying reagents reduced both ODC activities, verifying the key roles of cysteine and lysine residues in the catalytic mechanism of ODC. ELISA was performed to characterize the immunological difference between the rat and plant ODC. Both the rat and N. glutinosa ODC were recognized by the polyclonal antibody that was raised against purified N. glutinosa ODC, but the rat ODC was 50-fold less sensitive to the antibody binding. These results indicate that even though both ODCs have the same evolutionary origin, there seems to be a structural distinction between the species.

• 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.

• Journal of Life Science
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• v.7 no.2
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• pp.149-159
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• 1997

Chitin, a linked polysaccharide composed of 2-acetamido-2-deoxy-$\beta$-D-glucopytanose residues, is distributed widely in nature. It has been utilized on various application field due to the development of chitin derivatives such as chitosan, partial deacetylated chitin, carboxylmethyl chitin, sulfated chitin, and so on. Chitin and chitosan have been recently interested in antitumor and antimicrobial activities, because of a powerful tumor inhibitory effect against experimental mouse tumors. Especially, the oligosaccharides obtained by partial degradation of them exhibited a remarkable antitumor effect against sarcoma 180, MM 48 and Meth Asolid tumors and antimetastatic effect against Lewis lung carcinoma in mice. This review describes on antitumor effects of chitin, chitosan and their oligosaccharides by their mechanism of action involving enhancement of immunological system.

• Proceedings of the Ginseng society Conference
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• 2002.10a
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• pp.366-375
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• 2002

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 (Foster and Chongxi, 1992). Modern human studies have investigated preventive effect of ginseng on several kinds of cancer (Yun et al, 1993,Yun, 1995,Yun and Choi, 1998), its long term immunological effect on HIV patients (Sankang, 1989, Cho et al, 1997), its effect on cell mediated immune functions in healthy volunteers (Scaglione et al, 1990). Similarly non clinical studies on animal model system have studied the chemopreventive action of ginseng on cancer (Kumar, 1993,98) and immunological properties of ginseng (Kim et al, 1990, Tomoda et al, 1993, Yun et al, 1993, Mizuno et al, 1994,Lee et al, 1997, Park et al, 2001,Yoshikawa et al, 2001, Wang et al, 2001). 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.

• IMMUNE NETWORK
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• v.2 no.2
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• pp.65-71
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• 2002

The immunological mechanism of the responses to ultraviolet (UV) B radiation in mouse models were investigated by the suppression of contact hypersensitivity (CHS) and delayed type hypersensitivity (DTH), and susceptibility to infection. However, there are some differences in immune suppression according to the different models as well as the irradiation protocols. Therefore, this review focused on the differences in the suppressive effects on CHS and DTH, and susceptibility to infection in relation to the different in vivo models. Recent advances in cytokine knockout mice experiments have the reexamination of the role of the critical cytokines in UVB-induced immune suppression, which was investigated previously by blocking antibodies. The characteristics of the suppressor cells responsible for UVB-induced tolerance were determined. The subcellular mechanism of UVB-induced immune suppression was also explained by the induction of apoptotic cells through the Fas and Fas-ligand interaction. The phagocytosis of the apoptotic cells is believed to induce the production of the immune suppressive cytokine like interleukin-10 by macrophages. Therefore, the therapeutic UVB response to a skin disease, such as psoriasis, by the depletion of infiltrating T cells could be considered in the extension line of apoptosis and immune suppression.