• Journal of the Korean Society of Food Science and Nutrition
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• v.25 no.2
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• pp.352-366
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• 1996

The nutritional status of host has a profound effect on immune response and its ability to defend aganinst invading pathogen. Almost all nutrient dificiencies impaired host defence, and more than recommended levels of certain nutrient enhance immune response beyond that observed with 'adequate'. But high-fat diets have been associated with various types of immune dysfunction in experimental animal models and humans. Also, high linoleic acid suppressed immune function and growth and metastasis of tumor than saturated fatty acids. The present review focused on the effect of dietary lipid on immune fuction, cytokine production and clinical conditions like infection, autoimmune disease and cancer.

• The Plant Pathology Journal
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• v.37 no.3
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• pp.268-279
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• 2021

Citrus scab, caused by the fungal pathogen Elsinoë fawcettii, is one of the most important fungal diseases affecting Citrus spp. Citrus scab affects young tissues, including the leaves, twigs, and fruits, and produces severe fruit blemishes that reduce the market value of fresh fruits. To study the molecular responses of satsuma mandarin (C. unshiu) to E. fawcettii, plant hormone-related gene expression was analyzed in response to host-compatible (SM16-1) and host-incompatible (DAR70024) isolates. In the early phase of infection by E. fawcettii, jasmonic acid- and salicylic acid-related gene expression was induced in response to infection with the compatible isolate. However, as symptoms advanced during the late phase of the infection, the jasmonic acid- and salicylic acid-related gene expression was downregulated. The gene expression patterns were compared between compatible and incompatible interactions. As scabs were accompanied by altered tissue growth surrounding the infection site, we conducted gibberellic acid- and abscisic acid-related gene expression analysis and assessed the content of these acids during scab symptom development. Our results showed that gibberellic and abscisic acid-related gene expression and hormonal changes were reduced and induced in response to the infection, respectively. Accordingly, we propose that jasmonic and salicylic acids play a role in the early response to citrus scab, whereas gibberellic and abscisic acids participate in symptom development.

• Journal of Microbiology and Biotechnology
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• v.29 no.12
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• pp.1873-1881
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• 2019

The innate immune response serves as a first-line-of-defense mechanism for a host against viral infection. Viruses must therefore subvert this anti-viral response in order to establish an efficient life cycle. In line with this fact, Kaposi's sarcoma-associated herpesvirus (KSHV) encodes numerous genes that function as immunomodulatory proteins to antagonize the host immune system. One such mechanism through which KSHV evades the host immunity is by encoding a viral homolog of cellular interferon (IFN) regulatory factors (IRFs), known as vIRFs. Herein, we summarize recent advances in the study of the immunomodulatory strategies of KSHV vIRFs and their effects on KSHV-associated pathogenesis.

• Clinical and Experimental Pediatrics
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• v.58 no.7
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• pp.239-244
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• 2015

The complement system is part of the innate immune response and as such defends against invading pathogens, removes immune complexes and damaged self-cells, aids organ regeneration, confers neuroprotection, and engages with the adaptive immune response via T and B cells. Complement activation can either benefit or harm the host organism; thus, the complement system must maintain a balance between activation on foreign or modified self surfaces and inhibition on intact host cells. Complement regulators are essential for maintaining this balance and are classified as soluble regulators, such as factor H, and membrane-bound regulators. Defective complement regulators can damage the host cell and result in the accumulation of immunological debris. Moreover, defective regulators are associated with several autoimmune diseases such as atypical hemolytic uremic syndrome, dense deposit disease, age-related macular degeneration, and systemic lupus erythematosus. Therefore, understanding the molecular mechanisms by which the complement system is regulated is important for the development of novel therapies for complement-associated diseases.

• Journal of Microbiology and Biotechnology
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• v.33 no.3
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• pp.288-298
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• 2023

Host defense peptides are expressed in various immune cells, including phagocytic cells and epithelial cells. These peptides selectively alter innate immune pathways in response to infections by pathogens, such as bacteria, fungi, and viruses, and modify the subsequent adaptive immune environment. Consequently, they play a wide range of roles in both innate and adaptive immune responses. These peptides are of increasing importance due to their broad-spectrum antimicrobial activity and their functions as mediators linking innate and adaptive immune responses. This review focuses on the pleiotropic biological functions and related mechanisms of action of human host defense peptides and discusses their potential clinical applications.

• IMMUNE NETWORK
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• v.16 no.3
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• pp.159-164
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• 2016

IL-33 is a multifunctional cytokine that is released in response to a variety of intrinsic and extrinsic stimuli. The role of IL-33 in Candida albicans infections is just beginning to be revealed. This cytokine has beneficial effects on host defense against systemic C. albicans infections, and it promotes resistance mechanisms by which the immune system eliminates the invading fungal pathogens; and it also elevates host tolerance by reducing the inflammatory response and thereby, potentially, tissue damage. Thus, IL-33 is classified as a cytokine that has evolved functionally to protect the host from damage by pathogens and immunopathology.

• Journal of Plant Biology
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• v.36 no.3
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• pp.285-292
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• 1993

Cellular compatibility in the self-parasitism of Cuscuta australis R. Brown was studied at the ultrastructural level. The front cells of the haustorium penetrated the host stems independently grew within the host tissues and transformed into elongate, filamentous hyphae. Each hyphal cells contained a large nucleus and dense cytoplasm with abundant cell organelles. Multilamellar structures were contained in the cytoplasm and cell walls of the penetrating hyphal cells. When the hyphal cells did not yet invade the host cells, the middle lamella and the fused cellulosic cell walls of the two partners at the host-parasite interface were preserved well. As the invasion of the parasitic hyphal cells progressed, however, the middle lamella was not found at the interface and the host cell walls and plasma membranes were partially broken down. A hyphal cell penetrated deeply into the host cell had a more darkly stained cytoplasm with numerous of cell organelles. In the host cells attacked by the hyphal cells the limiting membranes of plastids were broken down and several vesicles were arrayed near the cell walls. No plasmodesmatal connections between the host and parasite cell walls were found; however, half-plasmodesmata were observed frequently on the side of the hyphal cell walls. These results suggested that the compatibility response in the self-parasitism of Cuscuta was expressed by cell walls, not by plasmodesmata, between the host and the parasite cells.

• IMMUNE NETWORK
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• v.14 no.3
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• pp.128-137
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• 2014

Respiratory viruses can induce acute respiratory disease. Clinical symptoms and manifestations are dependent on interactions between the virus and host immune system. Dendritic cells (DCs), along with alveolar macrophages, constitute the first line of sentinel cells in the innate immune response against respiratory viral infection. DCs play an essential role in regulating the immune response by bridging innate and adaptive immunity. In the steady state, lung DCs can be subdivided into $CD103^+$ conventional DCs (cDCs), $CD11b^+$ cDCs, and plasmacytoid DCs (pDCs). In the inflammatory state, like a respiratory viral infection, monocyte-derived DCs (moDCs) are recruited to the lung. In inflammatory lung, discrimination between moDCs and $CD11b^+$ DCs in the inflamed lung has been a critical challenge in understanding their role in the antiviral response. In particular, $CD103^+$ cDCs migrate from the intraepithelial base to the draining mediastinal lymph nodes to primarily induce the $CD8^+$ T cell response against the invading virus. Lymphoid $CD8{\alpha}^+$ cDCs, which have a developmental relationship with $CD103^+$ cDCs, also play an important role in viral antigen presentation. Moreover, pDCs have been reported to promote an antiviral response by inducing type I interferon production rather than adaptive immunity. However, the role of these cells in respiratory infections remains unclear. These different DC subsets have functional specialization against respiratory viral infection. Under certain viral infection, contextually controlling the balance of these specialized DC subsets is important for an effective immune response and maintenance of homeostasis.

• BMB Reports
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• v.43 no.4
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• pp.279-283
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• 2010

Polydnavirus genome is segmented and dispersed on host wasp chromosome. After replication, the segments form double- stranded circular DNAs and embedded in viral coat proteins. These viral particles are delivered into a parasitized host along with parasitoid eggs. A serine-rich protein (SRP) is predicted in a polydnavirus, Cotesia plutellae bracovirus (CpBV), genome in its segment no. 33 (CpBV-S33), creating CpBV-SRP1. This study explored its expression and physiological function in the diamondback moth, Plutella xylostella, larvae parasitized by C. plutellae. CpBV-SRP1 encodes 122 amino acids with 26 serines and several predicted phosphorylation sites. It is persistently expressed in all tested tissues of parasitized P. xylostella including hemocyte, fat body, and gut. Its physiological function was analyzed by injecting CpBV-S33 and inducing its expression in nonparasitized P. xylostella by a technique called SERI (segment expression and RNA interference). The expression of CpBV-SRP1 significantly impaired the spreading behavior and total cell count of hemocytes of treated larvae. Subsequent RNA interference of CpBV-SRP1 rescued the immunosuppressive response. This study reports the persistent expression of CpBV-SRP1 in a parasitized host and its parasitic role in suppressing the host immune response by altering hemocyte behavior and survival.

• Genomics & Informatics
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• v.3 no.3
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• pp.63-67
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• 2005

Adaptive responses to diverse microbial pathogens might be limited in relatively few types. Host cell responses to pathogens are believed to be patterned or stereotyped along with species or class. We tried to compose the host response to Mycoplasma in terms of cellular gene expression. Although gene expression profile of two host HeLa and 293 cells were quite different each other, 30 genes were differentially expressed by mycoplasma infection in both of HeLa and 293 cells. Six of them (PR48, MADH4, MKPX, CRK, RBM7, NEK3) were related to cell cycle or proliferation. Another category of genes like IL1 HY1, KLRF1, TNFSF14, GBP1 were host defense to elicit immune responses. With this set of genes, we establish the prediction model for mycoplasma contamination.