• Molecules and Cells
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• 제44권5호
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• pp.281-291
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• 2021

Tissue-resident macrophages play an important role in maintaining tissue homeostasis and innate immune defense against invading microbial pathogens. Brain-resident macrophages can be classified into microglia in the brain parenchyma and non-parenchymal brain macrophages, also known as central nervous system-associated or border-associated macrophages, in the brain-circulation interface. Microglia and non-parenchymal brain macrophages, including meningeal, perivascular, and choroid plexus macrophages, are mostly produced during embryonic development, and maintained their population by self-renewal. Microglia have gained much attention for their dual roles in the maintenance of brain homeostasis and the induction of neuroinflammation. In particular, diverse phenotypes of microglia have been increasingly identified under pathological conditions. Single-cell phenotypic analysis revealed that microglia are highly heterogenous and plastic, thus it is difficult to define the status of microglia as M1/M2 or resting/activated state due to complex nature of microglia. Meanwhile, physiological function of non-parenchymal brain macrophages remain to be fully demonstrated. In this review, we have summarized the origin and signatures of brain-resident macrophages and discussed the unique features of microglia, particularly, their phenotypic polarization, diversity of subtypes, and inflammasome responses related to neurodegenerative diseases.

• IMMUNE NETWORK
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• 제23권3호
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• pp.23.1-23.17
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• 2023

Inflammation is a series of host defense processes in response to microbial infection and tissue injury. Inflammatory processes frequently cause extracellular acidification in the inflamed region through increased glycolysis and lactate secretion. Therefore, the immune cells infiltrating the inflamed region encounter an acidic microenvironment. Extracellular acidosis can modulate the innate immune response of macrophages; however, its role for inflammasome signaling still remains elusive. In the present study, we demonstrated that macrophages exposed to an acidic microenvironment exhibited enhanced caspase-1 processing and IL-1β secretion compared with those under physiological pH. Moreover, exposure to an acidic pH increased the ability of macrophages to assemble the NLR family pyrin domain containing 3 (NLRP3) inflammasome in response to an NLRP3 agonist. This acidosis-mediated augmentation of NLRP3 inflammasome activation occurred in bone marrow-derived macrophages but not in bone marrow-derived neutrophils. Notably, exposure to an acidic environment caused a reduction in the intracellular pH of macrophages but not neutrophils. Concordantly, macrophages, but not neutrophils, exhibited NLRP3 agonist-mediated translocation of chloride intracellular channel protein 1 (CLIC1) into their plasma membranes under an acidic microenvironment. Collectively, our results demonstrate that extracellular acidosis during inflammation can increase the sensitivity of NLRP3 inflammasome formation and activation in a CLIC1-dependent manner. Thus, CLIC1 may be a potential therapeutic target for NLRP3 inflammasome-mediated pathological conditions.

• IMMUNE NETWORK
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• 제1권1호
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• pp.70-76
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• 2001

Background: Rheumatoid arthritis is an autoimmune disease characterized by a chronic inflammatory process, primarily involving the synovial membrane of peripheral j oints, where T cell activation is found. To address the superantigen stimulation in rheumatoid arthritis, T cell clonality and the expression of activation markers were analyzed. Methods: To detect TCRB V usage, inverse PCR and sequencing were done. Monoclonal antibodies were used for flow cytometric analysis of TCRBV8 or TCRBV5. As results, a restricted usage of TCRBV3 gene was detected in synovial lymphocytes from one rheumatoid arthritis patient. However, preferential usage for TCRB V8, which may be one indicator for stimulation by staphylococcal superantigen, was not obvious although general activation of T cells was found as high DR+ percentage in synovial T cells. These data show specific antigen rather than superantigen might involve the pathogenesis of rheumatoid arthritis.

• IMMUNE NETWORK
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• 제4권4호
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• pp.224-228
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• 2004

Background: The expression of BRG1 associated factors (BAF) 155 and BAF 170 in response to $IFN-{\gamma}$ or $TNF-{\alpha}$ was studied in astrocytoma cell lines and primary astrocytes. BAFs are complexed with BRG1 and are also associated with activated glucocorticoid for glucocorticoid trans-activation. Methods: $IFN-{\gamma}$ was pretreated for 18 hrs and cells were incubated with IL-1 or $TNF-{\alpha}$ for 72 hrs or 96 hrs with different concentrations of steroid. Cell death was measured by LDH assay. BAF expression was assayed by RT-PCR. Results: $IFN-{\gamma}$ increased cell death by dexamethasone in LN215 cells but not in LN319 cells. The $IFN-{\gamma}$ increased the expression of BAF 155 and BAF 170 in adult astrocytes and LN215 cells, but $IFN-{\gamma}$ decreased the expression of BAF 155/170 in LN319 cells. The effect of $IFN-{\gamma}$ on the expression of BAF was not as clear in fetal astrocytes as it was in adult astrocytes. Conclusion: Our results suggest cytokines produced during immune reaction or immunotherapy may modulate steroid susceptibility of astrocytes and astrocytoma cells by influencing the expression of BAFs.

• BMB Reports
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• 제48권12호
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• pp.696-701
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• 2015

Toll-like receptor 3 (TLR3) recognizes viral double-stranded RNA. It stimulates pro-inflammatory cytokine and interferon production. Here we reported the expression of a novel isoform of TLR3 in human astrocyte cell lines whose message is generated by alternative splicing. The isoform represents the N-terminus of the protein. It lacks many of the leucine-rich repeat domains, the transmembrane domain, and the intracellular Toll/interleukin-1 receptor domain of TLR3. Type I interferons (interferon-α and interferon-β) induced the expression of this isoform. Exogenous overexpression of this isoform inhibited interferon regulatory factor 3, signal transducers and activators of transcription 1, and Inhibitor of kappa B α signaling following stimulation. This isoform of TLR3 also inhibited the production of chemokine interferon-γ-inducible protein 10. Our study clearly demonstrated that the expression of this isoform of TLR3 was a negative regulator of signaling pathways and that it was inducible by type I interferons. We also found that this isoform could modulate inflammation in the brain.

• 한국가금학회:학술대회논문집
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• 한국가금학회 2002년도 가을 학술발표논문집
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• pp.90-91
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• 2002

사료 중 크릴밀이 브로일러의 생산성과 단백질 및 에너지 이용성에 미치는 영향을 조사하기 위하여 0일령 병아리(Avian종)에 기초사료와 기초사료중 대두박을 대치한 크릴밀 사료를 3주간 급여하여 2주째에 2일에 한번씩 LPS로 면역 자극하였다. 병아리의 일당 증체와 사료섭취량은 크릴사료의 영향은 없었으나 면역스트레스시 유의하게(p〈0.05) 낮아졌다. 간장과 비장무게는 면역스트레스시 급여사료 중 크릴 함량에 관계없이 유의하게 높았다. 질소밸런스는 면역스트레스시 유의하게 낮았으나 사료 중 크릴함량의 영향은 관찰되지 않았다. 사료 g당 대사에너지값은 면역스트레스시 높아지는 경향이 있었으나 면역스트레스가 없으면 낮아지는 경향이 있었다. 뇨산배설량은 면역스트레스시 크릴사료를 급여하면 높아지는 경향이 있었다.

• 한국환경성돌연변이발암원학회지
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• 제26권3호
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• pp.89-92
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• 2006

To enhance our understanding of immunological stimulating effects through the pathway by which nitric oxide (NO) activity and alkaline phosphatase(ALP) enzyme activity from the marine algae, Ulva lactuca, we have investigated NO activity by using mouse RAW264.7 cell line. And ALP enzyme activity performed by spleen of ICR mouse. The results showed that NO activity of the $H_2O$ fraction is the most effective than activities of other solvent fractions.

• 대한한의학회지
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• 제22권1호
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• pp.3-9
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• 2001

In the view of oriental medicine, the liver is the general of the army in its function of protecting against the enemy. So this concept is very closely associated to the immunological function. Its relations with immunological function are as follows. 1. The liver produces most of the proteins and converts them with hepatocytes, composes 80% in total reticuloendothelial system with Kuffer cells & endothelial cells and has typical structure of sinusoidal vessels closely related with the blood system. 2. The liver plays an important role in innate immunity with Kuffer cells as well as with the molecules that the liver produces, related to complementary systems. 3. In the embryonic period, the liver is associated with immune associated cell growth and their maturation. After birth, it is associated with removing old red blood cells and with systematically modulating immune system through hormone metabolism. 4. The liver controls the autoimmune disease resulting from immune complex by removing molecules like immune complex. 5. In the processing of blood 19A from the digestive system, the liver has an important role in protecting the body from unnecessary immune responses. 6. In the oriental medical view, liver plays a major role in the immune function by storing blood and dispersing stagnated hepatoqi with the help of the kidneys and spleen.

• 대한약침학회지
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• 제7권3호
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• pp.27-35
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• 2004

Beevenom immunotherapy(BVIT) in allergic patients is a well-established treatment modality for the prevention of systemic anaphylactic reactions caused by insect stings. BVIT is accompanied by increases in allergen-specific IgG, particularly the IgG4 isotype, which blocks not only IgE-dependent histamine release from basophils but also IgE-mediated antigen presentation to T cells. Inhibition of T cells after BVIT also involves decreased induction of the costimulatory molecule ICOS, which, in turn, seems to be dependent on the presence of IL-10, also associated with the inhibited status of T cells after BVIT. Suppression of T cells by IL-10 is an active process, which depends on the expression and participation of CD28. Immune tolerance in specific allergen immunotherapy might be a consequence of decreased Th2 or increased Th1 response of allergen specific T lymphocytes. BVIT shifted cytokine responses to allergen from a TH-2 to a TH-1 dominant pattern, suggesting direct effects on T cells. Many studies showed that severe side effects due to venom immunotherapy are rare. These results suggest that immunological changes after BVIT may be applied to be therapeutic alternative of general allergic diseases including beevenom allergy.

• Asian-Australasian Journal of Animal Sciences
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• 제22권3호
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• pp.350-355
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• 2009

Arachidonic acid (AA) is a polyunsaturated fatty acid that is a normal constituent of membrane lipids in animal cells. In addition to its role as a precursor of prostaglandins, AA itself may play an important role in the regulation of cell function. The effect of AA on functions of granulosa cells was investigated in pre-hierarchical small yellow follicles of laying hens. Immuno-cytochemical staining showed that AA ($10^{-7}-10^{-5}$ M) increased the expression of the extracellular matrix glycoprotein laminin, gap junction connexin 43 and protein kinase C (PKC). Therefore, mediated by the PKC signal pathway, AA may regulate the intercellular communication of granulosa cells and follicular development by increasing the expression of laminin and connexin.