• IMMUNE NETWORK
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• v.14 no.2
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• pp.67-72
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• 2014

The herpes virus entry mediator (HVEM) is a member of the tumor necrosis factor receptor superfamily (TNFRSF), and therefore it is also known as TNFRSF14 or CD270 (1,2). In recent years, we have focused on understanding HVEM function in the mucosa of the intestine, particularly on the role of HVEM in colitis pathogenesis, host defense and regulation of the microbiota (2-4). HVEM is an unusual TNF receptor because of its high expression levels in the gut epithelium, its capacity to bind ligands that are not members of the TNF super family, including immunoglobulin (Ig) superfamily members BTLA and CD160, and its bi-directional functionality, acting as a signaling receptor or as a ligand for the receptor BTLA. Clinically, Hvem recently was reported as an inflammatory bowel disease (IBD) risk gene as a result of genome wide association studies (5,6). This suggests HVEM could have a regulatory role influencing the regulation of epithelial barrier, host defense and the microbiota. Consistent with this, using mouse models, we have revealed how HVEM is involved in colitis pathogenesis, mucosal host defense and epithelial immunity (3,7). Although further studies are needed, our results provide the fundamental basis for understanding why Hvem is an IBD risk gene, and they confirm that HVEM is a mucosal gatekeeper with multiple regulatory functions in the mucosa.

• Journal of Dairy Science and Biotechnology
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• v.28 no.1
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• pp.35-41
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• 2010

Food allergy is defined as adverse reactions toward food mediated by aberrant immune mechanisms. Therefore, an allergic response to a food antigen can be thought of as an aberrant mucosal immune response. Food allergy most often begins in the first 1~2 years of life with the process of sensitization by which the immune system responds to specific food proteins, most often with the development of allergen-specific immunoglobulin E (IgE). Over time, most food allergeies are lost, although allergy to some foods is often long lived. The most important allergen sources involved in early food allergy are milk, eggs, peanut, soybean, meat, fish and cereals. Milk allergy seem to be associated with casein and whey protein. Important features of proteins as allergenicity are size, abundance and stability. Strategies for the prevention of milk allergy is breast-feeding, partially hydrolysised infant formula, using of probiotics, immune components in milk, preparation of low allergenicity milk protein and allergy therapy (immune therapy).

• Korean Journal of Food Science and Technology
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• v.43 no.1
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• pp.72-76
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• 2011

The adjuvant effects of Korean mistletoe lectin-C (KML-C) were investigated following the oral administration of KML-C with ovalbumin (OVA) as an antigen. Mice were orally immunized with OVA alone or admixed with various doses of KML-C or cholera toxin (CT), and the titer of OVA-specific antibody in the serum and mucosal secretions were determined. OVA+KML-C-treated mice showed high titers of IgA specific to CT in mucosal secretions. The antibody titers in the serum of OVA+KML-C-treated mice were comparable to those in the serum of OVA+CT-treated mice. When mice were immunized with OVA+KML-C or with CT alone and subsequently injected with OVA on the footpads after the primary immunization, they showed a more significant increase in delayed-type hypersensitivity reactions than when they were administered CT alone. These results suggest that KML-C is a potent immunoadjuvant that enhances both humoral and cellular immunity by the mucosal immune system.

• Journal of the korean veterinary medical association
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• v.29 no.8
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• pp.449-461
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• 1993

• Journal of the korean veterinary medical association
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• v.30 no.12
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• pp.710-728
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• 1994

이 논문은 국내에서의 새로운 vaccine의 연구 및 개발에 참고가 되었으면 하는 뜻에서, D.T.O'Hagan저 'Novel Delivery Systems for Oral vaccines'(CRC Press, 1994) 서적 중의 소개문을 번역한 것입니다.

• IMMUNE NETWORK
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• v.23 no.1
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• pp.7.1-7.27
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• 2023

The mammalian intestines harbor trillions of commensal microorganisms composed of thousands of species that are collectively called gut microbiota. Among the microbiota, bacteria are the predominant microorganism, with viruses, protozoa, and fungi (mycobiota) making up a relatively smaller population. The microbial communities play fundamental roles in the maturation and orchestration of the immune landscape in health and disease. Primarily, the gut microbiota modulates the immune system to maintain homeostasis and plays a crucial role in regulating the pathogenesis and pathophysiology of inflammatory, neuronal, and metabolic disorders. The microbiota modulates the host immune system through direct interactions with immune cells or indirect mechanisms such as producing short-chain acids and diverse metabolites. Numerous researchers have put extensive efforts into investigating the role of microbes in immune regulation, discovering novel immunomodulatory microbial species, identifying key effector molecules, and demonstrating how microbes and their key effector molecules mechanistically impact the host immune system. Consequently, recent studies suggest that several microbial species and their immunomodulatory molecules have therapeutic applicability in preclinical settings of multiple disorders. Nonetheless, it is still unclear why and how a handful of microorganisms and their key molecules affect the host immunity in diverse diseases. This review mainly discusses the role of microbes and their metabolites in T helper cell differentiation, immunomodulatory function, and their modes of action.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.19 no.4
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• pp.221-228
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• 2016

The gastrointestinal exposome represents the integration of all xenobiotic components and host-derived endogenous components affecting the host health, disease progression and ultimately clinical outcomes during the lifespan. The human gut microbiome as a dynamic exposome of commensalism continuously interacts with other exogenous exposome as well as host sentineling components including the immune and neuroendocrine circuit. The composition and diversity of the microbiome are established on the basis of the luminal environment (physical, chemical and biological exposome) and host surveillance at each part of the gastrointestinal lining. Whereas the chemical exposome derived from nutrients and other xenobiotics can influence the dynamics of microbiome community (the stability, diversity, or resilience), the microbiomes reciprocally alter the bioavailability and activities of the chemical exposome in the mucosa. In particular, xenobiotic metabolites by the gut microbial enzymes can be either beneficial or detrimental to the host health although xenobiotics can alter the composition and diversity of the gut microbiome. The integration of the mucosal crosstalk in the exposome determines the fate of microbiome community and host response to the etiologic factors of disease. Therefore, the network between microbiome and other mucosal exposome would provide new insights into the clinical intervention against the mucosal or systemic disorders via regulation of the gut-associated immunological, metabolic, or neuroendocrine system.

• IMMUNE NETWORK
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• v.4 no.2
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• pp.73-80
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• 2004

Viruses are obligate intracellular parasites which cause infection by invading and replicating within cells. The immune system has mechanisms which can attack the virus in extracellular and intracellular phase of life cycle, and which involve both non-specific and specific effectors. The survival of viruses depends on the survival of their hosts, and therefore the immune system and viruses have evolved together. Immune responses to viral infection may be variable depending on the site of infection, the mechanism of cell-to-cell spread of virus, physiology of the host, host genetic variation, and environmental condition. Viral infection of cells directly stimulates the production of interferons and they induce antiviral state in the surrounding cells. Complement system is also involved in the elimination of viruses and establishes the first line of defence with other non-specific immunity. During the course of viral infection, antibody is most effective at an early stage, especially before the virus enters its target cells. The virus- specific cytotoxic T lymphocytes are the principal effector cells in clearing established viral infections. But many viruses have resistant mechanism to host immune responses in every step of viral infection to cells. Some viruses have immune evasion mechanism and establish latency or persistency indefinitely. Furthermore antibodies to some viruses can enhance the disease by the second infection. Immune responses to viral infection are very different from those to bacterial infection.

• Journal of Plant Biotechnology
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• v.37 no.3
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• pp.250-261
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• 2010

The expression of vaccine antigens in transgenic plants has the potential to provide a convenient, stable, safe approach for oral vaccination alternative to traditional parenteral vaccines. Over the past two decades, many different vaccine antigens expressed via the plant nuclear genome have elicited appropriate immunoglobulin responses and have conferred protection upon oral delivery. Up to date, efforts to produce antigen proteins in plants have focused on potato, tobacco, tomato, banana, and seed (maize, rice, soybean, etc). The choice of promoters affects transgene transcription, resulting in changes not only in concentration, but also in the stage tissue and cell specificity of its expression. Inclusion of mucosal adjuvants during immunization with the vaccine antigen has been an important step towards the success of plant-derived vaccines. In animal and Phase I clinical trials several plant-derived vaccine antigens have been found to be safe and induce sufficiently high immune response. Future areas of research should further characterize the induction of the mucosal immune response and appropriate dosage for delivery system of animal and human vaccines. This article reviews the current status of development in the area of the use of plant for the development of oral vaccines.

• Food Science of Animal Resources
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• v.34 no.6
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• pp.829-835
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• 2014

Inflammatory bowel disease (IBD) is caused by dysregulation of colon mucosal immunity and mucosal epithelial barrier function. Recent studies have reported that lipoteichoic acid (LTA) from Lactobacillus plantarum K8 reduces excessive production of pro-inflammatory cytokine. In this study, we investigated the preventive effects of lysate of Lb. plantarum K8 in dextran sulfate sodium (DSS)-induced colitis. Male Sprague-Dawley rats were orally pretreated with lysate of Lb. plantarum K8 (low dose or high dose) or live Lb. plantarum K8 prior to the induction of colitis using 4% DSS. Disease progression was monitored by assessment of disease activity index (DAI). Histological changes of colonic tissues were evaluated by hematoxylin and eosin (HE) staining. Tumor necrosis factor-alpha (TNF-${\alpha}$), interleukin-6 (IL-6) levels were measured using enzyme-linked immunosorbent assay (ELISA). The colon mRNA expressions of TNF-${\alpha}$, IL-6, and toll like receptor-2 (TLR-2) were examined by quantitative real-time-transcription polymerase chain reaction (qPCR). Lysate of Lb. plantarum K8 suppressed colon shortening, edema, mucosal damage, and the loss of DSS-induced crypts. The groups that received lysate of Lb. plantarum K8 exhibited significantly decreased levels of the pro-inflammatory cytokines TNF-${\alpha}$ and IL-6 in the colon. Interestingly, colonic expression of toll like receptor-2 mRNA in the high-dose lysate of Lb. plantarum K8 group increased significantly. Our study demonstrates the protective effects of oral lysate of Lb. plantarum K8 administration on DSS-induced colitis via the modulation of pro-inflammatory mediators of the mucosal immune system.