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Muñoz, Roldan Melba Lucia. "Interferon gamma inducible protein 10 (IP-10) and regulatory T Cells in leishmaniasis". College Park, Md.: University of Maryland, 2007. http://hdl.handle.net/1903/7336.
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Thesis (M.S.) -- University of Maryland, College Park, 2007.Thesis research directed by: Dept. of Cell Biology and Molecular Genetics. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Beier, Stefanie [Verfasser]. "Entwicklung eines IP-10 Bioassays zur Bestimmung der Interferon Sensitivität / Stefanie Beier". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2007. http://d-nb.info/1022580183/34.
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Campos, Mauricio de Souza. "Níveis de citocinas plasmáticas em indivíduos com hepatite b crônica naive e sob tratamento antiviral". Instituto de Ciências da Saúde, 2014. http://repositorio.ufba.br/ri/handle/ri/17932.
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PRONEX e CAPES
Introdução: A infecção pelo vírus da hepatite B (HBV) compreende um amplo espectro de quadros clínicos que vai desde a manifestação aguda e autolimitada até a forma crônica, com possibilidade de desenvolvimento de cirrose hepática e carcinoma hepatocelular. A proteína 10 induzida por INF-γ (IP-10) é uma quimiocina CXC que pode ser secretada pelos hepatócitos e endotélio sinusoidal no fígado de pacientes com hepatite viral. Por ligação ao receptor CXCR3, IP-10 exerce efeito quimiotático em células NK, células T ativadas e células dendríticas, modulando, dessa forma, a resposta imunológica. Sabe-se que o IFN-γ estimula a secreção de IP-10 por células infectadas pelo vírus da hepatite C, mas no contexto da infecção pelo HBV, essa relação ainda é pouco conhecida. Objetivo: descrever os níveis das citocinas e quimiocinas séricas em pacientes com hepatite B crônica naive e sob tratamento antiviral. Material e métodos: foi realizada a dosagem de citocinas séricas de 24 voluntários com hepatite B crônica em tratamento e 33 voluntários com hepatite B crônica naive, utilizando o kit de CBA (Citokine Beads Array) da eBioscience e análise em FACScalibur BD. A citocina IP-10 foi quantificada utilizando o kit CBA da empresa BD conforme padronização prévia e recomendação do fabricante, e também analisada em FACScalibur BD. Os softwares SPSS versão 18 e GraphPad versão 6 foram utilizados para análise estatística. Resultados: foram encontradas diferenças estatísticas na comparação dos níveis de IP-10, IL-5 e TGF – β entre indivíduos com hepatite B crônica tratados e naive. Foram encontrados valores mais elevados de citocinas Th1 no soro de pacientes naive, quando comparados aos pacientes tratados. Os níveis séricos de IP-10 nos pacientes tratados e não tratados são mais elevados que os de INF-γ. Conclusão: os níveis séricos de citocinas Th1 entre pacientes não tratados estavam mais elevados do que em pacientes tratados. A amplitude dos níveis de INFγ foi maior nas amostras dos indivíduos com hepatite B sem tratamento. A correlação entre os níveis de INFγ e IL- 10 foi inversa em amostras de indivíduos não tratados. O tratamento pareceu modular a produção de INFγ sem interferir nos níveis de IP-10 e IL-10. A correlação entre os níveis de IP-10 e IL-10 também foi inversa em amostras de indivíduos não tratados. A IP-10 pode ser um marcador de maior sensibilidade que o INF-gama anteriormente descrito como a citocina chave no processo inflamatório na HBV
Background: infection with the hepatitis B virus(HBV) comprises a broad spectrum of clinical presentations ranging from acute and self-limited to the chronic form, with the possibility of development of liver cirrhosis and hepatocellular carcinoma. The protein10 induced by INF-γ(IP-10) is a CXC chemokine that can be secreted by hepatocytes and sinusoidal endothelium in the liver of patients with viral hepatitis. By binding to CXCR3 receptor, IP-10 exerts a chemotactic effect on NK cells, activated T cells and dendritic cells, potentializing, thus, the immune response. It is known that IFN-γ stimulates IP-10 secretion by cells infected with hepatitis C, but in the context of HBV infection, this relationship is still poorly known. Aim: to describe the levels of cytokines and chemokines in serum patients with chronic hepatitis B naïve and under antiviral treatment. Methods: the dosage of serum cytokines of 24 volunteers with chronic hepatitis B treatment and 33 volunteers with chronic hepatitis B naïve was performed using the CBA kit (Citokine Beads Array) from eBioscience and analyzed using FACScalibur BD. IP-10 cytokine was quantified using the CBA kit from BD company as previous standardization and recommendation of the manufacturer and also analyzed using FACScalibur BD. The SPSS software version 18 and GraphPad version 6 were used for statistical analysis. Results: statistical differences were found when comparing the IP-10 levels, IL-5 and TGF-β among individuals with chronic hepatitis B treated and naive. Higher values of Th1cytokines were found in the serum of treated patients when compared to naïve patients. The IP-10 serum levels in treated and untreated patients are higher than those of INF-γ. Conclusion: the serum levels of Th1cytokines from untreated patients were higher than in patients treated. The breadth of the INFγ levels were higher in samples of individuals without hepatitis B treatment. The correlation between the levels of INFγ and IL-10 was reverse on samples from untreated individuals. The treatment appeared to modulate INFγ production without interfering on IP-10and IL-10 production levels. The correlation between the IP-10 and IL-10 levels was also reverse in samples of untreated individuals. IP-10 may be a higher sensibility marker than the INFγ priorly described as a key cytokine in the inflammatory process in hepatitis B.
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Alsleben, Neele. "Der Biomarker IP-10 für die Diagnose der aktiven Tuberkulose und der latenten Tuberkuloseinfektion im Kindesalter". Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-168313.
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Einleitung: Zur in-vitro Diagnostik der Tuberkulose (TB) und latenten TB Infektion (LTBI) im Kindesalter werden derzeit zunehmend „Interferon-gamma (IFN-γ) release assays“ (IGRA) verwendet. Die Sensitivität der IGRA insbesondere im Kindesalter ist umstritten. Auch eine diagnostische Unterscheidung zwischen TB und LTBI ist mittels IGRA und anderen bisherigen basierten Testverfahren nicht möglich. In vorangegangen Studien zeigte sich der Biomarker „IFN-γ-inducible-protein-10“ (IP-10) als viel versprechend zur Diagnose der TB und LTBI.
Ziele: In der vorliegenden Dissertationsschrift wurden die IP-10-Plasmakonzentrationen von Kindern mit TB, LTBI, Atemwegsinfektion (AWI) oder nicht-tuberkulöse Mykobakterien (NTM)-Erkrankung ohne Stimulation der Proben, nach unspezifischer Mitogen-Stimulation und nach spezifischer Mycobacterium tuberculosis (M. tuberculosis)-Antigen-Stimulation bestimmt. Die Antigen-stimulierten IP-10-Plasmakonzentrationen der TB- und LTBI-Gruppe wurden mit denen der NTM- und AWI-Gruppe verglichen. Darüberhinaus wurde beurteilt, ob eine Unterscheidung zwischen TB und LTBI anhand der IP-10-Plasmakonzentration möglich ist. Außerdem wurde die Konkordanz und Korrelation zwischen dem IP-10-ELISA und QuantiFERON® -TB Gold In-Tube (QFT-IT) Test beurteilt und untersucht, ob der Biomarker IP-10 altersabhängig sezerniert wird.
Material & Methoden: 48 Kinder wurden in die Studie eingeschlossen. Das mittlere Alter der Studienteilnehmer war 54 Monate. Alle Studienteilnehmer wurden zuvor in Deutschland entweder mit einer TB (n=11), LTBI (n=14), NTM (n=8) oder AWI (n=15) diagnostiziert. Unabhängig von der vorliegenden Studie wurden bei allen teilnehmenden Kindern IFN-γ-Werte mittels des QFT-IT-Testes bestimmt. Im Rahmen des QFT-IT wurden die für den Test notwendigen Blutproben entweder nicht stimuliert, mit einer unspezifischen Mitogenen-Substanz oder mit spezifischen M.tuberculosis-Antigenen stimuliert. Die jeweiligen Plasma-Überstände wurden asserviert und zur Bestimmung von IP-10 verwendet. Die IP-10-Konzentrationen wurden, in Zusammenarbeit mit dem Klinischen Forschungszentrums der Universität von Kopenhagen, mittels einem zu Forschungszwecken entwickelten ELISAs gemessen.
Ergebnisse: Die IP-10-Plasmakonzentrationen ohne Stimulation, mit unspezifischer Mitogen- und spezifischer Antigen-Stimulation betrug für die TB-Gruppe 704 pg/ml, 12.966 pg/ml und 12.702 pg/ml; für die LTBI-Gruppe 366,5 pg/ml, 10.232 pg/ml und 9.109 pg/ml; für die NTM-Gruppe 309 pg/ml, 11.197 pg/ml und 97 pg/ml; und für die AWI-Gruppe 694 pg/ml, 5.401 pg/ml und 84 pg/ml. Es konnte kein signifikanter Unterschied zwischen der IP-10-Konzentration der TB- und LTBI-Gruppe festgestellt werden (p-Wert= 0,24). Die IP-10- und IFN-γ- Plasmakonzentrationen der Kinder mit TB und LTBI korrelierten stark miteinander (rsp=0,65; p-Wert = 0,03 und rsp=0,79; p-Wert < 0,001). Der IP-10-ELISA und QFT-IT Test zeigten ebenso eine hohe Konkordanz (κ =0,96). Die IP-10-Sekretion war 18fach höher im Vergleich zur IFN-γ-Sekretion. Es konnte keine Korrelation zwischen dem Alter und der Mitogen-stimulierten IP-10-Konzentration nachgewiesen werden.
Schlussfolgerungen: Die IP-10-Plasmakonzentration von Kindern mit TB und LTBI im Vergleich zu Kindern mit NTM und AWI ist signifikant nach spezifischer M.tuberculosis-Antigen-Stimulation erhöht (p-Wert > 0,001). Die qualitativen und quantitativen Testergebnisse des IP-10-ELISAs korrelieren stark mit denen des QFT-IT-Testes. Im Vergleich zu IFN-γ scheint IP-10 in höheren Konzentrationen und möglicherweise unabhängig vom Alter sezerniert zu werden. Das legt die Vermutung nahe, dass IP-10 zur Diagnose der TB und LTBI im Kindesalter in Zukunft Verwendung finden könnte.
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Enderlin, Marta. "Evaluation of IP-10 and TNFalpha-transducing parvoviral vectors as antitumoral agents in animal glioblastoma models". [S.l. : s.n.], 2005. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB11759090.
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Carew, Jennifer S., Claudia M. Espitia, Weiguo Zhao, Monica M. Mita, Alain C. Mita i Steffan T. Nawrocki. "Oncolytic reovirus inhibits angiogenesis through induction of CXCL10/IP-10 and abrogation of HIF activity in soft tissue sarcomas". IMPACT JOURNALS LLC, 2017. http://hdl.handle.net/10150/625966.
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The tumor-selective viral replication capacity and pro-apoptotic effects of oncolytic reovirus have been reported to be dependent on the presence of an activated RAS pathway in several solid tumor types. However, the mechanisms of selective anticancer efficacy of the reovirus-based formulation for cancer therapy (Reolysin, pelareorep) have not been rigorously studied in soft tissue sarcomas (STS). Here we report that Reolysin triggered a striking induction of the anti-angiogenic chemokine interferon-gamma-inducible protein 10 (IP-10)/CXCL10 (CXC chemokine ligand 10) in both wild type and RAS mutant STS cells. Further analysis determined that Reolysin treatment possessed significant anti-angiogenic activity irrespective of RAS status. In addition to CXCL10 induction, Reolysin dramatically downregulated the expression of hypoxia inducible factor (HIF)-1 alpha, HIF-2 alpha and inhibited vascular endothelial growth factor (VEGF) secretion. CXCL10 antagonism significantly diminished the anti-angiogenic effects of Reolysin indicating that it is a key driver of this phenomenon. Xenograft studies demonstrated that Reolysin significantly improved the anticancer activity of the anti-angiogenic agents sunitinib, temsirolimus, and bevacizumab in a manner that was associated with increased CXCL10 levels. This effect was most pronounced following treatment with Reolysin in combination with temsirolimus. Further analysis in additional sarcoma xenograft models confirmed the significant increase in CXCL10 and increased anticancer activity of this combination. Our collective results demonstrate that Reolysin possesses CXCL10-driven anti-angiogenic activity in sarcoma models, which can be harnessed to enhance the anticancer activity of temsirolimus and other agents that target the tumor vasculature.
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Hubel, Silvia [Verfasser]. "Untersuchung der Biomarker Interferon-gamma induziertes Protein 10 (IP-10) und CXC-Motiv-Chemokinrezeptor 3 (CXCR3) im Plasma nierentransplantierter Patienten in den ersten fünfzehn Monaten nach Transplantation / Silvia Hubel". Tübingen : Universitätsbibliothek Tübingen, 2020. http://d-nb.info/1218073640/34.
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Rose, Thomas [Verfasser]. "IFNα and its response proteins, IP-10 and SIGLEC-1, are biomarkers of disease activity in systemic lupus erythematosus / Thomas Rose". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/1052222056/34.
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Alsleben, Neele [Verfasser], i Holger [Akademischer Betreuer] Rüssmann. "Der Biomarker IP-10 für die Diagnose der aktiven Tuberkulose und der latenten Tuberkuloseinfektion im Kindesalter / Neele Alsleben. Betreuer: Holger Rüssmann". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1050647890/34.
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Su, Yung-Chang University of New South Wales & Garvan Institute of Medical Research St Vincent's Clinical School UNSW. "Immune regulation in mouse models of allergic asthma". Awarded by:University of New South Wales & Garvan Institute of Medical Research. St. Vincent's Clinical School, 2006. http://handle.unsw.edu.au/1959.4/26978.
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Allergic asthma is an immunological disease, mediated by CD4+ Th2 cells, and its prevalence has increased over recent decades. Features of allergic asthma include airway hyperresponsiveness (AHR), airway eosinophilia, excessive airway mucus production, and increased IgE and Th2 cytokine levels. Airway remodeling with pulmonary fibrosis is noted in the progress of asthma. In this thesis, a murine model of allergic asthma was used to investigate the effect of cyclophosphamide (CY) on asthma and the involvement of regulatory T cells (Treg), and the role of Granulocyte-macrophage colony stimulating-factor (GM-CSF) in allergic asthma by using GM-CSF knockout mice. CY is a cytotoxic agent, which paradoxically augments several immune responses. The first part of this thesis was aimed to study the effects of CY in a murine model of allergic airway inflammation. BALB/c mice were immunized with ovalbumin (OVA) on days 0 and 14, and challenged with aerosolized OVA from days 21 to 27. Some mice additionally received CY on days -2 and 12. In the CY-treated animals, pronounced worsening of inflammatory features was noted, including increases in eosinophil infiltration, epithelial thickness, mucus occlusion and eosinophil numbers in bronchoalveolar lavage fluid (BALF). Increased total and OVA-specific serum IgE were also noted in the CY-treated animals. In cell cultures from peritracheal lymph nodes, the Th2 cytokines IL-4 and IL-5 were elevated in animals treated with CY. It was hypothesized that the effects of CY could be caused by reduced immunosuppression mediated by Treg. mRNA expression of the immunosuppressive cytokines IL-10 and TGF-beta was reduced in the lungs of CY-treated mice. The expression of FoxP3, a marker of naturally occurring Treg, was significantly reduced in spleens, thymuses and peritracheal lymph nodes after the second injection of CY, and in the lung tissue after allergen challenge in CY-treated mice. Furthermore, lung IL-10-producing CD4+ T cells and CTLA-4+-bearing CD4+ T cells were reduced after allergen aerosol challenge in CY-treated mice. Thus CY worsened the features of allergic pulmonary inflammation in this model, in association with increased production of IgE and Th2 cytokines. The reduction in expression of FoxP3 and immunosuppressive cytokines by CY suggests that toxicity to Treg may contribute to the increased inflammation. GM-CSF plays a role in the growth, development, and maturation of bone marrow hemopoietic cells into mature blood cells, and has been proposed to be involved in potentiating the function of inflammatory cells in allergic inflammation. In the second part of this thesis, GM-CSF knockout (KO) mice were used to investigate the role of GM-CSF. In allergic KO mice, airway eosinophils were only shown in the perivascular, but not peribronchial areas in the lung, compared to the allergic wild-type (WT) mice in which eosinophil infiltration appeared in both areas. Eosinophil numbers were drastically reduced in the bronchoalveolar lavage fluid (BALF) of KO mice. IL-5 production in the lung tissue and BALF in allergic KO mice was reduced; similar results were also found in peritracheal draining lymph nodes after in vitro stimulation assays. However, IL-4 and IL-13 production, airway hyperresponsiveness (AHR), and serum IgE production were not affected in allergic KO mice. Surprisingly, lung IFN-gamma mRNA and BALF levels were increased in allergic KO mice. Lung mRNA levels of CCR3, a key chemokine receptor on eosinophils, were significantly reduced in allergic KO mice, whereas expression of the chemokines eotaxin and RANTES were at similar levels in allergic KO and WT mice. Lung mRNA levels of the IFN-gamma-inducible chemokines Mig (CXCL9) and IP-10 (CXCL10), which are antagonists of CCR3, and their receptor CXCR3 were increased in allergic KO mice, compared with allergic WT mice. Data obtained from flow cytometry showed more eosinophils survived in the lung of WT mice than KO mice. Another allergy model, a peritoneal allergy model was performed to investigate inflammation in a different model. Leukocyte subpopulations such as neutrophils, eosinophils, macrophages, and lymphocytes were reduced in the peritoneal lavage fluid of allergic KO mice. The findings revealed that GM-CSF is essential for IL-5 production, pulmonary airway eosinophilia and eosinophil survival. In the absence of GM-CSF, over-production of IFN-???? may induce chemokines, including Mig and IP-10, which are antagonists for CCR3 and may reduce airway eosinophil infiltration. In this thesis, a murine model of allergic asthma has been used to obtain novel findings on the regulation of allergic inflammation. The results with CY are relevant to the treatment of asthma patients with CY and other cytotoxic agents. The findings in the GM-CSF KO mice suggest that GM-CSF is a potential therapeutic target in asthma, and that in assessment of new therapeutic agents for asthma, effects on GM-CSF should be considered.
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Stumpfe, Florian Matthias Maximilian [Verfasser], i Udo [Akademischer Betreuer] Jeschke. "Zytokinbestimmung im Verlauf der Schwangerschaft und deren Bedeutung bei intrauterinen Infektionen : Konzentrationsbestimmung der Zytokine Interleukin-6, Interleukin-15, pro-Interleukin-1β und CXCL10/IP-10 im Fruchtwasser / Florian Matthias Maximilian Stumpfe. Betreuer: Udo Jeschke". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1050647920/34.
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Vasireddi, Mugdha. "Subversion of Natural Killer Cell Defenses Induced by a Deadly Zoonotic Virus". Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/biology_diss/65.
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B virus (Macacine herpesvirus 1, Cercopithecine herpesvirus 1, herpes B virus) is an Old World monkey simplex virus endemic in macaques. B virus infection in its natural host, macaque, is very similar to HSV-‐1 infection in humans causing mild or asymptomatic infection. On the other hand, zoonotic infection in humans results in death in the absence of early initiation of antiviral drugs. Viruses evade host immune responses in order to survive and propagate. Most herpes viruses including HSV-‐1 down-‐regulate major histocompatibility complex class I (MHC class I) surface expression on infected cells in order to prevent CD8+ T-‐cell recognition and subsequent cell lysis. MHC class I molecules bind to the inhibitory receptors of NK cells and prevent NK cell activity. Thus, this mechanism protects HSV-‐1 infected cells from CD8+ T-‐cell lysis, making them sensitive to natural killer (NK) cell cytotoxicity. To investigate if B virus pathogenicity is a result of novel immune evasion mechanisms employed by B virus, we determined NK cell regulation during B virus infection. To this end, our experiments demonstrate that B virus does not down-‐ regulate MHC I expression as effectively as HSV-‐1, leading us to hypothesize that B virus in-‐ fected cells are resistant to NK cell activity. We examined the expression of MHC I chain related genes (MICA/ MICB), which are activation ligands to NKG2D receptors on NK cells. Our results show that there is no significant difference in MICA and MICB expression between HSV-‐1 and B virus infected cells. Furthermore, we tested for the up-‐regulation of cytokines and chemokines responsible for NK cell activation and migration. Our results indicate a significant up-‐regulation of IFN-‐α from PBMCs co-‐cultured with HSV-‐1 infected cells, which plays an important role in activating NK cells. NK cells within these PBMCs up-‐regulate perforin release indicative of NK cell activity. PBMCs co-‐cultured with B virus infected cells do not up-‐regulate any cytokines or chemokines responsible for NK cell activity. As a result the NK cells within these PBMCs do not significantly up-‐regulate perforin release. These results demonstrate that B virus employs a novel immune evasion mechanism to subvert NK cell activity.
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Harris, Daniel Pellerin. "PRMT5-CATALYZED ARGININE METHYLATION OF NF-kappaB p65 INTHE ENDOTHELIAL CELL INDUCTION OF PRO-INFLAMMATORYCHEMOKINES". Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1449579234.
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CARMO, A. P. "Solução Segura para Utilização de VPN Baseada em IP´s Dinâmicos". Universidade Federal do Espírito Santo, 2010. http://repositorio.ufes.br/handle/10/9591.
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Previous issue date: 2010-06-14Nessa pesquisa, estudamos a anatomia cerebral, os padrões oscilatórios dos circuitos neurais do sistema tálamo-cortical e sugerimos um modelo para as fontes cerebrais baseado em dipolos elétricos, então, calculamos atenuação do campo elétrico e formamos um sistema de equações lineares para separar os sinais de EEG linearmente misturados no Encéfalo. Esse método foi testado em classificadores baseados em regras, classificadores estatísticos (Análise por Discriminante Quadrático, Análise por Discriminante Linear e Análise por Discriminante Regularizado) e redes neurais artificiais durante a classificação de 3 tarefas mentais, relacionadas à imaginação de movimento das mãos direita/esquerda e a geração de palavras começando com uma mesma letra qualquer.
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Huang, Mei-Liang, i 黃美椋. "Analysis of human interferon-gamma-inducible protein 10 (IP-10)/CXCL10 promoter polymorphism at position -938". Thesis, 2007. http://ndltd.ncl.edu.tw/handle/95334133739233112603.
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博士臺灣大學
流行病學研究所
95
Introduction - Interferon-γ inducible protein 10 (IP-10)/CXCLl10 was shown to be an indicator of disease progress for severe acute respiratory syndrome (SARS); a high plasma level in the early clinical stage was associated with subsequent adverse outcome. The mechanism that triggers CXCL10 expression in SARS-CoV infection is still unknown. Method - We conducted a genetic epidemiological study to identify the single nucleotide polymorphism (SNP) of CXCL10 that might be associated with severe SARS clinical outcomes. With luciferase assay and electromobility shift assay (EMSA), we conducted in vitro functional study of the polymorphic alleles of CXCL10 promoter with the attempt to identify the regulatory factors for CXCL10 expression. Results - Five SNPs of CXCL10 were typed for 108 SARS patients along with 242 healthy control DNAs. A genotype TT at the CXCL10(-938) SNP locus was identified to correlate with severity of SARS-CoV infected patients, especially among SARS patients with a detectably higher nasopharyngeal virus load. DNA fragment of the 996 bp upstream of the CXCL10 start codon containing either (-938C) or (-938T) SNP was cloned into the luciferase reporter pGL3 vector along with a series of 5’ end truncated CXCL10 promoter DNA fragments. With IFN-γ stimulation in A549 cell and HMEC-1 cells, the shortest two fragments (-704, and -413) showed a high luciferase activity, which dropped with each increment of the 5’ end DNA length; stimulation with IFN-γ and TNF-α in combination induced a higher luciferase activity, but the drop of activity was reversed with the fragment of -704 and -996, suggesting possibly IFN-γ associated negative regulation factors and TNF-α associated positive regulation factors could bind to this region. The difference of luciferase activity between the two alleles of CXCL10(-996C) and CXCL10(-996T) could not be consistently demonstrated, however. We used nuclear extracts from IFN-γ induced THP-1 cells and the 32P-labeled probes of CXCL10(-928~-948) promoter sequence containing (-938C) or (-938T) and antibodies against a number of TFs antibodies to perform EMSA. The (-938C) probe consistently binds to more nuclear proteins than the (-938T) probe, and three putative binding proteins, YY-1, MZF and Pax-6, of CXCL10 (-938) were found to reduce the shifted band in EMSA and supershift assay. The activation functions of YY-1 and MZF on CXCL10 expression were demonstrated by luciferase assay and the results showed YY-1 and MZF could trigger the activation of CXCL10, however, YY-1 and MZF induced activity were not different between the two alleles. Conclusion - The genotype TT of CXCL10 (-938) SNP was associated with adverse outcome of SARS patient. The DNA sequence flanking the CXCL10 (-938) SNP locus possibly contain binding motifs of YY-1, MZF and Pax-6. However, the functional difference between these two alleles of CXCL10 (-938) could not be demonstrated in vitro by luciferase assay and EMSA in the study.
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Hsieh, Ming-Fang, i 謝明芳. "The Roles of CXCR3 and CXCL10/IP-10 in Dengue Virus Infection". Thesis, 2005. http://ndltd.ncl.edu.tw/handle/97102048436394937920.
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碩士國立陽明大學
微生物及免疫學研究所
93
Dengue virus (DV), a member of flavivirus, is an arthropod-born human pathogen. Dengue virus contains a positive-single strand genomic RNA that is translated as a polyprotein. The polyprotein is processed by proteases into ten discrete proteins-three structure proteins and seven non-structure proteins. We have previously shown that the CXCL10/IP-10 expression was predominantly induced in mice following dengue virus infection. In this study, we have investigated the role of CXCL10/IP-10 in dengue virus infection. CXCL10/IP-10 is an inflammatory chemokine and mediates the recruitment of activated T cells and NK cells that express the CXCR3 chmokine receptor. Ligands for CXCR3 include CXCL10/IP-10 as well as CXCL9/Mig and CXCL11/I-TAC. Given that CXCL10/IP-10 is a highly positive charged molecule able to bind to heparan sulfate (HS) and that heparan sulfate is a putative receptor for dengue virus, we thereby hypothesize that CXCLI0/IP-10 may compete with dengue virus for binding to heparan sulfate on cell surface. We found that CXCL10/IP-10 was able to inhibit dengue virus binding to cell surface. Furthermore, we demonstrated that the CXCL10/IP-10 mutant protein in which the putative amino acid residues critical for binding to heparan sulfate were mutated failed to inhibit dengue virus binding to cell surface. This result indicates that the inhibitory effect of CXCL10/IP-10 on dengue virus biding to cells is likely due to CXCL10/IP-10 competing with dengue virus for biding to haparan sulfate on cell surface. We further examined the importance of CXCR3 and CXCL10/IP-10 in dengue virus infection by in vivo study. When mice were infected intracerebrally with dengue virus, CXCR3-deficient mice showed significantly higher mortality as compared with wild-type mice. Of interest, the surviving CXCR3-deficient mice, but not wild-type mice, developed paralysis. Both wild-type and CXCR3-deficeint mice began to show detectable virus in the brain at day 3 and viral loads peaked at day 5-6 post-infection, with significantly higher levels in CXCR3-deficient mice. Only the CXCR3-deficient mice had detectable virus in the spinal cord, peaking at day 5. The viral load coincided with the mortality, indicating that CXCR3-deficient mice had the impaired ability on viral clearance in the central nervous system, leading to neuronal damage and subsequently paralysis and/or death. Of particular interest, we found that the mortality of CXCL10/IP-10-deficient mice was similar to that of CXCR3-deficient mice. Given that ligands for CXCR3 are CXCL9/Mig, CXCL10/IP-10 and CXCL11/I-TAC and that in vitro activation of CXCR3 by these ligands gives similar functional activity, it would be expected that CXCL9/Mig and CXCL11/I-TAC should be able to compensate CXCL10/IP-10’s function in CXCL10/IP-10-deficient mice. However, our results suggest that the in vivo fuction of CXCL10/IP-10 is indispensable following dengue virus infection. Collectively, the results on animal study suggest that both CXCR3 and CXCL10/IP-10 play critical roles in resistance to primary dengue virus infection and that the function of chemokine in vivo may not be redundant.
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Huang, Kuo-Hsiung, i 黃國雄. "Mechanisms Underlying the Mycobacterium Tuberculosis Mediated IP-10 (IFN-gamma-inducible protein 10 kD) expression in Human Monocytic cells". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/63257263896236070297.
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博士臺北醫學大學
醫學科學研究所
102
C-X-C chemokines, such as IP-10 (CXCL10, IFN-gamma-inducible Protein 10 kD) and IL-8 (CXCL8, Interleukin 8) play critical roles in the immunopathogenesis of pulmonary against Mycobacterium tuberculosis (M. Tb) at the pathologic site(s). NF-kappaB repressing factor (NRF) is a transcriptional silencer and has been reported to bind in negative regulatory element (NRE) site and implicated in the basal silencing of IL-8 genes. We checked and found a similar NRE site in IP-10 gene promoter region. To understand the regulatory role of NRF in IP-10 release on pulmonary TB, we studied the alveolar macrophages (AM) and peripheral blood mononuclear cells (PBMC) derived from patients with active TB and normal subjects, and THP-1 cell line, respectively. The Amplified Mycobacterium Tuberculosis Direct (AMTD) test showed that the bacterial loads in AM of pulmonary TB patients in terms of ribosomal RNA were highly compatible with sputum bacterial load of M. Tb. Using confocal image analysis, western blot and quantitative real-time PCR, we demonstrated that the protein and mRNA levels of IP-10 and NRF were significantly higher in AM, PBMC in patients with active pulmonary TB and THP-1 cells treated with heated Tuberculosis bacilli (H. TB), respectively. And the release of IP-10 is mediated via NF-kappaB (p65). In PBMC, the chromatin immunoprecipitation (ChIP) assay showed a higher binding of NRF to IP-10 promoter sites in TB patients with high bacterial load compared to low bacterial load or normal subjects. The ChIP assay in THP-1 cell treated with H. TB showed NRF binding to IP-10 promoter sites was higher in high dose H. TB group. NRF knockdown (SiNRF) significantly increased the release of IP-10 from PBMC of TB patients with high bacterial load than normal subjects. SiNRF can also increase the release of IP-10 in normal subjects’ PBMC and THP-1 cells treated with H. TB, significantly. Using p-CMV6-XL4-NRF (p-CMV-NRF), overexpression NRF inhibited NF-kappaB-mediated IP-10 synthesis and release in active pulmonary TB patients’ PBMC and THP-1 cells treated with H. TB, respectively. In active pulmonary TB patients’ AM and PBMC, the repressive effect of NRF is mediated via interference with NF-kappaB (p65) binding and recruitment to promoter sites of IP-10. NRF downregulated IP-10 basal expression and H. TB induced IP-10 synthesis via interference with NF-kappaB (p65) binding and RNA polymerase II recruitment to IP-10 promoter site in THP-1 cells. Taken together the present results, we not only reveal the mechanism in NRF modulate M. Tb induced IP-10 release for the first time, but also provide a possible therapeutic strategies in the regulation of NRF to helping pulmonary TB patients.
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Yang, Che-Wen, i 楊哲文. "The roles of IP-10 in the pathogenesis of severe cutaneous adverse drug reactions". Thesis, 2017. http://ndltd.ncl.edu.tw/handle/rsqp3f.
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碩士國立臺灣大學
臨床醫學研究所
105
The clinical manifestations of cutaneous adverse drug reactions (cADRs) encompass a wide spectrum of clinical severity, ranging from benign maculopapular eruption (MPE) to severe cutaneous adverse reactions (SCARs). As one of the SCARs, drug reaction with eosinophilia and systemic symptoms (DRESS) involves several unique features, including delayed onset, fever, rash, lymphadenopathy, hematological abnormalities, systemic illness, and prolonged courses. In recent years, a number of studies have focused in particular on sequential human herpes virus 6 (HHV-6) reactivation in DRESS. From our published data, the HHV-6 reactivation rate was 43.5% in DRESS group but not in other cADR patients. DRESS patients with HHV-6 reactivation usually have more severe presentations, more frequent flaring courses, and prolonged illness compared to those without HHV-6 reactivation. When compared with DRESS patients without HHV-6 reactivation and SJS/TEN patients, IL-1Ra, IL-1β, IL-6 and TNF-α levels at acute stage were significantly lower in DRESS patients with HHV-6 reactivation, and IP-10 level was significantly higher. The above mentioned findings have raised our interest to explore the role of IP-10 in the pathomechanism of DRESS. In this study, we aim to investigate the roles of IP-10 in cutaneous pathology, immunological mechanisms and HHV-6 reactivation among patients with DRESS and SJS. A prospective study had been conducted since September 2010 to May 2016 at NTUH. Hospitalized patients who were diagnosed as having DRESS or SJS/TEN by dermatologists were included. Clinical and laboratory data were collected and analyzed. Skin biopsy specimens were prepared for immunohistochemistry staining with IP-10 and CXCR3. From 66 DRESS patients, we found a higher IP-10 level among those with HHV-6 reactivation. Lower B cell counts at acute stage were detected in patients with DRESS but not in those with SJS/TEN. In this prospective cohort, the chronic complications encountered in DRESS patients include Hashimoto’s thyroiditis, followed by type 1 diabetes mellitus (DM) and long-term dialysis resulting from the worsening of pre-existing renal failure. Compared with SJS skin lesions, more abundant IP-10+ and CXCR3+ cells were demonstrated in DRESS skin biopsies on immunohistochemistry analysis. There were significantly higher percentage of CXCR3+CD4+ T cells、CXCR3+CD8+ T cells and CXCR3+CLA+ cells in the PBMCs of patients of DRESS, consistent with histological findings. The results from this study suggest the IP-10/CXCR3 axis may participate to a different extent in the skin inflammatory process of DRESS and SJS/TEN.
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Nawka, Peter. "Überprüfung eines Serumproteinprofils für die Diagnostik von Glioblastomen". Doctoral thesis, 2013. http://hdl.handle.net/11858/00-1735-0000-0001-BC2F-4.
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Die Diagnostik eines Glioblastoms (GBM) stützt sich z.Z. neben klinischer Symptomatik auf bildgebende Diagnostik sowie die histologische Untersuchung. In letzter Zeit werden zuneh-mend Serumproteine beschrieben und untersucht, die mit einer GBM-Erkrankung assoziiert sind. Elstner, Stockhammer und Kollegen haben 2011 ein Serumproteinprofil identifiziert, das aus CXCL10/IP-10, BMP-2 und HSP70 besteht und in einem Kollektiv von 23 GBM-Erkrankten und 9 Gesunden eine Sensitivität von 89% und eine Spezifität von 96% besaß. Dieses Profil wurde nun in einer unizentrischen klinischen Studie an 35 GBM-Erkrankten und 37 Patienten mit differenzialdiagnostisch relevanten Erkrankungen (v. a. Hirnmetastasen und primären ZNS-Lymphomen) überprüft. Dabei wurden die präoperativ abgenommenen Blut-proben mittels des ELISA-Nachweisverfahrens untersucht und die jeweiligen Konzentratio-nen in die von Elstner et al. (2011) entwickelte Regel eingesetzt. In diesem Kollektiv konnte das Profil nicht zwischen einem GBM und seinen Differenzialdiagnosen unterscheiden (Sensitivität 31%, Spezifität 54%). Es ist nicht als Hilfsmittel zur Diagnostik von Glioblastomen geeignet.
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Quante, Markus [Verfasser]. "Genexpression des Chemokinrezeptors CXCR3 und seiner Liganden Mig und IP-10 in der Frühphase nach allogener Nierentransplantation / vorgelegt von Markus Quante". 2008. http://d-nb.info/989793737/34.
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Enderlin, Marta [Verfasser]. "Evaluation of IP-10 and TNFα-transducing [TNF-alpha-transducing] parvoviral vectors as antitumoral agents in animal glioblastoma models / presented by Marta Enderlin". 2005. http://d-nb.info/97446712X/34.
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Vlachakis, Dimitrios P. "Zur Rolle der Chemokine IP-10, MIG und I-TAC bei der Rekrutierung von T-Lymphozyten in das Lungengewebe von Patienten mit Sarkoidose und anderen granulomatösen Lungenerkrankungen /". 2005. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=015045388&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
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Sabelhaus, Anne [Verfasser]. "Modulation der Chemokine IP-10 und MCP-1 und ihrer Rezeptoren CXCR3 bzw. CCR2 durch Interferon-β1a [Interferon-beta-1-a] in vitro und in vivo / vorgelegt von Anne Sabelhaus". 2007. http://d-nb.info/982863845/34.
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Jodoin, Danielle. "Le "sacrifice" du Christ et le "sacrifice" des chrétiens dans la Lettre aux Romains et la Première lettre de Pierre : incidences herméneutiques d'une approche synchronique axée sur les métaphores et l'intertextualité". Thèse, 2009. http://hdl.handle.net/1866/6704.
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Mußil, Bianka. "Charakterisierung der angeborenen Immunantwort in SIV-infizierten Rhesusaffen". Doctoral thesis, 2009. http://hdl.handle.net/11858/00-1735-0000-0006-AD8F-C.
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Khan, Sajjad. "Differential gene expression of chemokines in KRAS and BRAF mutated colorectal cell lines: Role of cytokines". Doctoral thesis, 2013. http://hdl.handle.net/11858/00-1735-0000-001D-BF64-6.
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Chen, Hsiu-Lin, i 陳秀玲. "Soluble form of the triggering receptor expressed on myeloid cells-1 (sTREM-1) and CXC chemokine IP-10 as diagnostic markers of serious bacterial infection in infants younger than 4 months of age". Thesis, 2006. http://ndltd.ncl.edu.tw/handle/86046193513893686321.
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碩士高雄醫學大學
醫學研究所碩士班
95
英文摘要 Background: Early diagnosis of serious bacterial infection (SBI) in young infants is a difficult problem by using clinical symptoms and signs. The goal of this study is to evaluate to diagnostic value of newly discovered inflammatory mediators: soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) or CXC chemokine IP-10 level for early diagnosis of SBI in infants younger than 4 months of age. Methods: We enrolled pediatric patients who were less than 4 months of age with a suspicion to have SBI and admitted in neonatal intensive care unit or complete nursing unit of pediatric department of Kaohsiung Medical University hospital. Peripheral blood was drawn for measurement of complete blood count, CRP, sTREM-1 or IP-10 levels at admission. Positive blood, CSF, or urine culture was considered to have SBI. Soluble TREM-1 and IP-10 were detected by commercial ELISA kits. Results: There were 118 patients to have sTREM-1 measurement. The SBI group (n=39) have higher plasma sTREM-1 level than non-SBI group (n=79) (299.8±555.4 v.s. 15.4±19.7，p=0.003 after adjusting age by ANCOVA analysis). Plasma sTREM-1 level higher than 55.2 ng/mL was more accurate than WBC count, absolute neutrophils counts, IT ratio, and CRP for indicating SBI in infants.[sensitivity 64.1% (95% CI, 55%-73%); specificity 97% (95% CI, 94%-100%); positive likelihood ratio 21.3; negative likelihood ratio 0.37; diagnostic odds ratio 57.5]。Sixty patients were collected to have measurement of IP-10. Plasma IP-10 level had significantly increase in SBI group [320.1±497.9 v.s. 11.6±23.7, p=0.016, after adjusting age by ANCOVA analysis] 。Plasma IP-10 level higher than 48.2 ng/mL had best diagnostic accuracy for indicating SBI. [sensitivity 81% (95% CI, 71%-90%); specificity 95% (95% CI 89%-100%); positive likelihood ratio 15.9，negative likelihood ratio 0.2; diagnostic odds ratio 79.3]。 Conclusion: In infants who were less than 4 months old, plasma sTREM-1 or IP-10 level might play a potential role in early identification of serious bacterial infection.