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  • 1
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    Online Resource
    Anti-inflammatory Activities and Component Change of Processed and Fermented Gastrodiae Rhizoma
    The American Association of Immunologists ; 2018
    In:  The Journal of Immunology Vol. 200, No. 1_Supplement ( 2018-05-01), p. 42.11-42.11
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 200, No. 1_Supplement ( 2018-05-01), p. 42.11-42.11
    Abstract: Gastrodiae Rhizoma (GR) is a traditional herbal medicine in Korea, China, and Japan, which has been used for the treatment of headaches, hypertension, oxidative stress, mental disorders, inflammation, and cardiovascular diseases. This study investigated the anti-infammatory activity and main component content of processed (PGR) and fermented Gastrodiae Rhizoma (FPGR). Processed method was soaked in vinegar solution until completely absorbed and steaming for 2 hours. Fermentation was carried out using Lactobacillus brevis and incubated at 37□ for 1~3 day. The anti-inflammatory activites were determine pro-inflammatory factors such as nuclear factor κB (NF-κB), nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in lipopolysaccharide (LPS)-induced RAW 264.7 cell line and major functional components (gastrodin, gastrodigenin, vanillylalcohol, p-hydroxybenzaldehyde) were also measured. The results showed that the FPGR reduced NO, PGE2, iNOS, COX-2, NF-κB production without cytotoxicity and improved major components. These results suggest that FPGR extracts may be a developed the functional food related to anti-inflammation due to the significant effects on inflammatory facters. Therefore, fermented and processed Gastrodiae Rhizoma can be useful methods which can help applied as functional resources in the industrial area.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.200.Supp.42.11
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2018
    detail.hit.zdb_id: 1475085-5
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  • 2
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    Online Resource
    Reactive Oxygen Species–Producing Myeloid Cells Act as a Bone Marrow Niche for Sterile Inflammation–Induced Reactive Granulopoiesis
    The American Association of Immunologists ; 2017
    In:  The Journal of Immunology Vol. 198, No. 7 ( 2017-04-01), p. 2854-2864
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 198, No. 7 ( 2017-04-01), p. 2854-2864
    Abstract: Both microbial infection and sterile inflammation augment bone marrow (BM) neutrophil production, but whether the induced accelerated granulopoiesis is mediated by a common pathway and the nature of such a pathway are poorly defined. We recently established that BM myeloid cell–derived reactive oxygen species (ROS) externally regulate myeloid progenitor proliferation and differentiation in bacteria-elicited emergency granulopoiesis. In this article, we show that BM ROS levels are also elevated during sterile inflammation. Similar to in microbial infection, ROS were mainly generated by the phagocytic NADPH oxidase in Gr1+ myeloid cells. The myeloid cells and their ROS were uniformly distributed in the BM when visualized by multiphoton intravital microscopy, and ROS production was both required and sufficient for sterile inflammation–elicited reactive granulopoiesis. Elevated granulopoiesis was mediated by ROS-induced phosphatase and tensin homolog oxidation and deactivation, leading to upregulated PtdIns(3,4,5)P3 signaling and increased progenitor cell proliferation. Collectively, these results demonstrate that, although infection-induced emergency granulopoiesis and sterile inflammation–elicited reactive granulopoiesis are triggered by different stimuli and are mediated by distinct upstream signals, the pathways converge to NADPH oxidase–dependent ROS production by BM myeloid cells. Thus, BM Gr1+ myeloid cells represent a key hematopoietic niche that supports accelerated granulopoiesis in infective and sterile inflammation. This niche may be an excellent target in various immune-mediated pathologies or immune reconstitution after BM transplantation.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1602006
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2017
    detail.hit.zdb_id: 1475085-5
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  • 3
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    Online Resource
    Immunosenescent characteristics of T cells in young patients following haploidentical stem cell transplantation from parental donors
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 87.26-87.26
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 87.26-87.26
    Abstract: Pediatric and adolescent patients in need of allogeneic hematopoietic stem cell transplantation (HSCT) generally receive stem cells from older, unrelated or parental donors when a sibling donor is not available. Despite encouraging clinical outcomes, it has been suggested that immune reconstitution accompanied by increased replicative stress and a large difference between donor and recipient age may worsen immunosenescence in pediatric recipients. Therefore, in this study paired samples were collected at the same time from donors and recipients of haploidentical hematopoietic stem cell transplantation (HaploSCT). We then conducted flow cytometry-based phenotypic and functional analyses and telomere length (TL) measurements of 21 paired T-cell sets from parental donors and children who received T cell-replete HaploSCT with post-transplant cyclophosphamide (PTCy). Senescent T cells, CD28− or CD57+ cells, were significantly expanded in patients. Further, not only CD4+CD28− T cells, but also CD4+CD28+ T cells showed reduced cytokine production capacity and impaired polyfunctionality compared with parental donors, whereas their TCR-mediated proliferation capacity was comparable. Of note, the TL in patient T cells was preserved, or even slightly longer, in senescent T cells compared with donor cells. Regression analysis showed that senescent features of CD4+ and CD8+ T cells in patients were influenced by donor age and the frequency of CD28− cells, respectively. Our data suggest that in pediatric HaploSCT, premature immunosenescent changes occur in T cells from parental donors and therefore, long-term immune monitoring should be conducted.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.87.26
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 4
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    Development of a DNA vaccine for SFTSV that confers complete protection against lethal infection in ferrets
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 167.33-167.33
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 167.33-167.33
    Abstract: Severe fever with thrombocytopenia syndrome (SFTS) is a newly emerging tick-borne infectious disease caused by the SFTS virus (SFTSV) belonging to the Phenuiviridae family. The WHO lists SFTSV as one of the most dangerous viral pathogens, and considers it likely to cause wide epidemics in the near future. The incidence of SFTSV infection has increased from its discovery in 2012 through 2018 with a mortality rate of 10–20% and the major clinical symptoms of SFTSV infection are fever, vomiting, diarrhea, thrombocytopenia, leukopenia and multiple organ failure. However, no effective vaccines are currently available for SFTSV. Here, we describe the development of a SFTSV-specific DNA vaccine, its immunogenicity, and its protective efficacy against SFTSV lethal challenge. Vaccine candidates induced both a neutralizing antibody response and multifunctional SFTSV-specific T cell response in mice and ferrets. To investigate the vaccine efficacy in vivo, we applied a recently developed ferret model of lethal infection that recapitulates fatal clinical symptoms in SFTSV infection in humans. Vaccinated ferrets were completely protected from lethal SFTSV challenge without developing any clinical signs. Moreover, we found that anti-envelope antibodies play an important role in protective immunity and non-envelope-specific T cell responses also can contribute to protection against SFTSV infection. This study provides important insights into the development of an effective vaccine, as well as corresponding immune parameters, to control SFTSV infection.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.167.33
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 5
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    PLAG ameliorates LPS-induced ALI by attenuation of neutrophil infiltration into alveolar via a prompt resolution of TLR4 signaling.
    The American Association of Immunologists ; 2018
    In:  The Journal of Immunology Vol. 200, No. 1_Supplement ( 2018-05-01), p. 42.3-42.3
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 200, No. 1_Supplement ( 2018-05-01), p. 42.3-42.3
    Abstract: Acute lung injury (ALI) is an acute respiratory failure that is associated with excessive neutrophil recruitment into the bronchoalveolar space and results in severe mortality. To evaluate 1-palmitoyl-2-linoleoyl-3-acetyl-rac-glycerol (PLAG) as a therapeutic agent for ALI, PLAG was administered orally to mice intranasally challenged with lipopolysaccharide (LPS). The excessive neutrophil infiltration in the bronchoalveolar lavage fluid (BALF) was detected in LPS-treated mice. Intranasally introduced LPS especially stimulates tissue-resident macrophages in the pulmonary tissue and induces neutrophil-attracting chemokine production such as MIP-2. Co-administrated PLAG dramatically ameliorated neutrophil infiltration into the bronchoalveolar region via modification of TLR4 signaling. We found that PLAG effectively accelerated endocytosis of LPS-TLR4 complex and promoted the NADPH oxidase activity through the formation of Rac, p47phox assembly into membrane for ROS production which results in elimination of exotoxin in Raw264.7 cells. PLAG also triggered a prompt TLR4 signals occurred in endosome mediated by TRIF and terminated signaling including MIP-2 expression when endocytosed exotoxin is cleared. Moreover, immunofluorescence microscopes of RAW264.7 cells showed that PLAG accelerated the endocytosis of the LPS-TLR4 complex and the clearance of the internalized LPS. Our results suggest that PLAG promotes the clearance of invaded exotoxin and eventually triggers an earlier termination of MIP-2 secretion in the exotoxin-cleared macrophages, and might be used as a potential therapeutic agent to prevent ALI through speedy resolution of exotoxin.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.200.Supp.42.3
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2018
    detail.hit.zdb_id: 1475085-5
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  • 6
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    Distinctive Dynamics and Functions of the CD4+CD25+FOXP3+ Regulatory T Cell Population in Patients with Severe and Mild COVID-19
    The American Association of Immunologists ; 2023
    In:  The Journal of Immunology Vol. 210, No. 11 ( 2023-06-01), p. 1687-1699
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 210, No. 11 ( 2023-06-01), p. 1687-1699
    Abstract: Although CD4+CD25+FOXP3+ regulatory T (TREG) cells have been studied in patients with COVID-19, changes in the TREG cell population have not been longitudinally examined during the course of COVID-19. In this study, we longitudinally investigated the quantitative and qualitative changes in the TREG cell population in patients with COVID-19. We found that the frequencies of total TREG cells and CD45RA−FOXP3hi activated TREG cells were significantly increased 15–28 d postsymptom onset in severe patients, but not in mild patients. TREG cells from severe patients exhibited not only increased proliferation but also enhanced apoptosis, suggesting functional derangement of the TREG cell population during severe COVID-19. The suppressive functions of the TREG cell population did not differ between patients with severe versus mild COVID-19. The frequency of TREG cells inversely correlated with SARS-CoV-2–specific cytokine production by CD4+ T cells and their polyfunctionality in patients with mild disease, suggesting that TREG cells are major regulators of virus-specific CD4+ T cell responses during mild COVID-19. However, such correlations were not observed in patients with severe disease. Thus, in this study, we describe distinctive changes in the TREG cell population in patients with severe and mild COVID-19. Our study provides a deep understanding of host immune responses upon SARS-CoV-2 infection in regard to TREG cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2200290
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2023
    detail.hit.zdb_id: 1475085-5
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  • 7
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    Role of platelet-activating factor in protecting against lipopolysaccharide-induced endotoxic shock (33.3)
    The American Association of Immunologists ; 2009
    In:  The Journal of Immunology Vol. 182, No. 1_Supplement ( 2009-04-01), p. 33.3-33.3
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 33.3-33.3
    Abstract: AbstractPlatelet-activating factor (PAF) has been long believed to be associated with many pathophysiological processes during septic shock. Here we present novel activities for PAF in the LPS-mediated endotoxic shock. In vivo PAF treatment immediately after LPS challenge markedly improved the survival rate against mortality from endotoxic shock. In addition, this treatment prominently attenuated LPS-induced profound hypotension, excessive polymorphonuclear neutrophil infiltration, severe multiple organ failure, and lymphocyte apoptosis. These protective effects of PAF was correlated with significantly decreases in the production of the inflammatory mediators such as TNF-α, IL-1β, IL-12, and IFN-γ, while increasing production of the anti-inflammatory cytokine IL-10 in vivo and in vitro. In response to LPS, PAF inhibits ERK1/2 and p38 MAPK activation, which is critical for proinflammatory cytokines production. Furthermore, PAF upregulates SOCS1 and SOCS3, which are essential for cross-talk inhibition in LPS-induced cytokine signaling. Taken together, these results suggest that PAF may provide protection against endotoxic shock via a complex mechanism involving modulation of inflammatory and anti-inflammatory mediators, as well as balanced regulation between activation and subsequent deactivation of the signaling pathways in response to LPS.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.182.Supp.33.3
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2009
    detail.hit.zdb_id: 1475085-5
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  • 8
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    STAT4 Expression in Human T Cells Is Regulated by DNA Methylation but Not by Promoter Polymorphism
    The American Association of Immunologists ; 2005
    In:  The Journal of Immunology Vol. 175, No. 11 ( 2005-12-01), p. 7143-7150
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 175, No. 11 ( 2005-12-01), p. 7143-7150
    Abstract: STAT4, which plays a pivotal role in Th1 immune responses, enhances IFN-γ transcription in response to the interaction of IL-12 with the IL-12R. Mice deficient in STAT4 lack IL-12-induced IFN-γ production and Th1 differentiation and display a predominantly Th2 phenotype. Although these findings indicate that STAT4 expression levels are important for the development of cytokine-producing Th1 cells, the transcriptional and posttranscriptional mechanisms regulating STAT4 expression are unknown. We sought to identify and characterize the transcriptional regulatory elements in the promoter region of the human STAT4 gene. We found that disruption of multiple transcriptional regions covering the CREB, OCT1, and SP1 motifs significantly reduced STAT4 promoter activity. However, genomic DNA isolated from 91 patients with asthma or rheumatoid arthritis showed no evidence of mutations in the defined STAT4 essential promoter region. The 5′ flanking region of the promoter was found to contain a −149A/G change in ∼20–35% of patients, but this polymorphism had no effect on promoter activity. Interestingly, STAT4 expression was drastically increased in human T cells following treatment with a DNA methyltransferase inhibitor, and truncation of methylation sites in the proximal regulatory elements of the STAT4 promoter markedly enhanced transcriptional activity. Thus, our findings provide molecular insight into STAT4 expression and suggest that, in human T cells, STAT4 expressional regulation is associated with DNA hypermethylation, but not promoter polymorphisms.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.175.11.7143
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2005
    detail.hit.zdb_id: 1475085-5
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  • 9
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    Online Resource
    The Effect of Vitamin C on the phenotype and function of Dendritic cells during activation with LPS (36.24)
    The American Association of Immunologists ; 2007
    In:  The Journal of Immunology Vol. 178, No. 1_Supplement ( 2007-04-01), p. S16-S17
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 178, No. 1_Supplement ( 2007-04-01), p. S16-S17
    Abstract: Activating DCs produce reactive oxygen species (ROS), which are necessary during antigen processing. In this study, we hypothesized that vitamin C (VC), as an antioxidant, may affect phenotype and function of DCs following activation. Bone marrow cells isolated from mice were cultured and differentiated into DCs in the presence of GM-CSF for 7 days. DCs were pre-treated with various concentrations of VC, and activated with LPS for 24 hrs. The supernatants were collected for measurements of cytokine secretion, and the changes of several markers of DC activation were analyzed. VC in the culture media reduced intracellular ROS levels, suggesting anti-oxidant effects on DCs. The expression of CD40 and CD80 were not influenced, but those of CD86 and MHC class II were slightly reduced. The reduction of phagocytic functions of DCs with activation was suppressed by the presence of VC, dose-dependently. In the supernatants, dose-dependent reduction of IL-6 and increased secretion of IL-12p70 and IL-10 were observed with increasing concentration of VC. IFN-¥ã was not detected at all. Because VC affected some of surface marker expression and phagocytic functions of activated DCs and, most noticeably, changed cytokine secretion profiles, we also investigated the results of T cell activation by those DCs treated with VC, with respect to T cell proliferation and cytokine secretion by activated T cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.178.Supp.36.24
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2007
    detail.hit.zdb_id: 1475085-5
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  • 10
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    Online Resource
    Protein Kinase CK2/PTEN Pathway Plays a Key Role in Platelet-Activating Factor-Mediated Murine Anaphylactic Shock
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 11 ( 2011-06-01), p. 6625-6632
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 11 ( 2011-06-01), p. 6625-6632
    Abstract: Platelet-activating factor (PAF) is a major mediator in the induction of fatal hypovolemic shock in murine anaphylaxis. This PAF-mediated effect has been reported to be associated with PI3K/Akt-dependent eNOS-derived NO. The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is phosphatidylinositol phosphate phosphatase, which negatively controls PI3K by dephosphorylating the signaling lipid, phosphatidylinositol 3,4,5-triphosphate. In this study, we examined the possible involvement of PTEN in PAF-mediated anaphylactic shock. Induction of anaphylaxis or PAF injection resulted in a rapid decrease in PTEN activity, followed by increases in PI3K activity and phosphorylation of Akt and eNOS. Systemic administration of adenoviruses carrying PTEN cDNA (adenoviral PTEN), but not the control AdLacZ, not only attenuated anaphylactic symptoms, but also reversed anaphylaxis- or PAF-induced changes in PTEN and PI3K activities, as well as phosphorylation of Akt and eNOS. We found that the decreased PTEN activity was associated with PTEN phosphorylation, the latter effect being prevented by the protein kinase CK2 inhibitor, DMAT. DMAT also inhibited anaphylactic symptoms as well as the anaphylaxis- or PAF-mediated PTEN/PI3K/Akt/eNOS signaling cascade. CK2 activity was increased by PAF. The present data provide, as the key mechanism underlying anaphylactic shock, PAF triggers the upstream pathway CK2/PTEN, which ultimately leads to the activation of PI3K/Akt/eNOS. Therefore, CK2/PTEN may be a potent target in the control of anaphylaxis and other many PAF-mediated pathologic conditions.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1100007
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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