Relevant bibliographies by topics / Interferon Gamma CXCL10

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Academic literature on the topic 'Interferon Gamma CXCL10'

Author: Grafiati
Published: 9 March 2023

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Journal articles on the topic "Interferon Gamma CXCL10"

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Hameed, Ruaa Salim. "Upregulated CXCL10 gene Expression in SARS-CoV-2 Infected people." BASRA JOURNAL OF SCIENCE 40, no. 2 (September 1, 2022): 357–65. http://dx.doi.org/10.29072/basjs.20220208.

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Interferon and interferon-induced genes play a crucial role in early-stage post-infection virus defense. C-X-C10, also known as interferon gamma-induced protein 10 or small-inducible cytokine B10, is encoded by the CXCL10 gene and is essential for T-helper cell recruitment. The purpose of this study was to assess the gene expression of CXCL10 in SARS-CoV-2-positive and -negative individuals using qPCR. The results demonstrated a 35-fold increase in CXCL10 expression in SARS-CoV-2-positive individuals vs to negative samples. In conclusion, the elevated gene expression of CXCL10 in SARS-CoV-2 patients is a signal for the immune system to respond to the invading virus and may be taken into account in the design of future vaccines.
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Lim, JaeHyun, Steven C. Derrick, Kristopher Kolibab, Amy Li Yang, Steven Porcelli, William R. Jacobs, and Sheldon L. Morris. "Early Pulmonary Cytokine and Chemokine Responses in Mice Immunized with Three Different Vaccines against Mycobacterium tuberculosis Determined by PCR Array." Clinical and Vaccine Immunology 16, no. 1 (November 26, 2008): 122–26. http://dx.doi.org/10.1128/cvi.00359-08.

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ABSTRACT In this study, the early pulmonary cytokine and chemokine responses in mice immunized with either BCG vaccine, a ΔsecA2 mutant of Mycobacterium tuberculosis, or a DNA vaccine expressing an ESAT6-antigen 85B fusion protein and then aerogenically challenged with a low dose of M. tuberculosis were evaluated by PCR array. The cellular immune responses at day 10 postchallenge were essentially equivalent in the lungs of mice immunized with either the highly immunogenic BCG vaccine or the ΔsecA2 M. tuberculosis mutant strain. Specifically, 12 immune biomolecules (including gamma interferon [IFN-γ], interleukin-21 [IL-21], IL-27, IL-17f, CXCL9, CXCL10, and CXCL11) were differentially regulated, relative to the levels for naïve controls, in the lungs of vaccinated mice at this time point. Although the vaccine-related immune responses evoked in mice immunized with the DNA vaccine were relatively limited at 10 days postinfection, upregulation of IFN-γ RNA synthesis as well as increased expression levels of CXCL9, CXCL10, and CXCL11 chemokines were detected.
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Schnabel, Christiane L., Susanna Babasyan, Heather Freer, and Bettina Wagner. "CXCL10 production in equine monocytes is stimulated by interferon-gamma." Veterinary Immunology and Immunopathology 207 (January 2019): 25–30. http://dx.doi.org/10.1016/j.vetimm.2018.11.016.

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Zaph, Colby, and Phillip Scott. "Interleukin-12 Regulates Chemokine Gene Expression during the Early Immune Response to Leishmania major." Infection and Immunity 71, no. 3 (March 2003): 1587–89. http://dx.doi.org/10.1128/iai.71.3.1587-1589.2003.

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ABSTRACT Following infection with Leishmania major, the chemokines XCL1, CXCL10, and CCL2 were preferentially expressed in draining lymph nodes of resistant mice. Neutralization of interleukin 12 (IL-12) or gamma interferon in resistant mice resulted in decreased chemokine expression, while administration of IL-12 to susceptible mice resulted in an increase in the level of chemokine gene expression.
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Colvin, Richard A., Gabriele S. V. Campanella, Lindsay A. Manice, and Andrew D. Luster. "CXCR3 Requires Tyrosine Sulfation for Ligand Binding and a Second Extracellular Loop Arginine Residue for Ligand-Induced Chemotaxis." Molecular and Cellular Biology 26, no. 15 (August 1, 2006): 5838–49. http://dx.doi.org/10.1128/mcb.00556-06.

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ABSTRACT CXCR3 is a G-protein-coupled seven-transmembrane domain chemokine receptor that plays an important role in effector T-cell and NK cell trafficking. Three gamma interferon-inducible chemokines activate CXCR3: CXCL9 (Mig), CXCL10 (IP-10), and CXCL11 (I-TAC). Here, we identify extracellular domains of CXCR3 that are required for ligand binding and activation. We found that CXCR3 is sulfated on its N terminus and that sulfation is required for binding and activation by all three ligands. We also found that the proximal 16 amino acid residues of the N terminus are required for CXCL10 and CXCL11 binding and activation but not CXCL9 activation. In addition, we found that residue R216 in the second extracellular loop is required for CXCR3-mediated chemotaxis and calcium mobilization but is not required for ligand binding or ligand-induced CXCR3 internalization. Finally, charged residues in the extracellular loops contribute to the receptor-ligand interaction. These findings demonstrate that chemokine activation of CXCR3 involves both high-affinity ligand-binding interactions with negatively charged residues in the extracellular domains of CXCR3 and a lower-affinity receptor-activating interaction in the second extracellular loop. This lower-affinity interaction is necessary to induce chemotaxis but not ligand-induced CXCR3 internalization, further suggesting that different domains of CXCR3 mediate distinct functions.
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Scollard, David M., Meher V. Chaduvula, Alejandra Martinez, Natalie Fowlkes, Indira Nath, Barbara M. Stryjewska, Michael T. Kearney, and Diana L. Williams. "Increased CXC Ligand 10 Levels and Gene Expression in Type 1 Leprosy Reactions." Clinical and Vaccine Immunology 18, no. 6 (April 20, 2011): 947–53. http://dx.doi.org/10.1128/cvi.00042-11.

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ABSTRACTType 1 reaction (T1R) is a systemic inflammatory syndrome causing substantial morbidity in leprosy. T1R results from spontaneously enhanced cellular immunity in borderline types of leprosy, but there are no established laboratory markers for the reaction. Preliminary studies have identified elevated circulating CXC ligand 10 (CXCL10) during T1R. Correlation of CXCL10 with clinical T1R was studied in repeated serum specimens obtained before, during, and after T1R. CXCL10 gene expression was assessed in biopsy specimens taken before and during T1R, and sections were stained for the cytokine using monoclonal antibodies. Sequential serum specimens revealed elevation of circulating CXCL10 associated with episodes of T1R (P= 0.0001) but no evidence of an earlier, predictive change in the level of the chemokine. Reverse transcriptase (RT)-PCR revealed elevated expression of CXCL10 transcripts during T1R, but not in patients who did not have T1R. No significant correlation between CXCL10 and gamma interferon (IFN-γ) mRNA levels was observed. Immunohistochemical staining of the skin biopsy specimens suggested an overall increase in CXCL10 but did not identify a particular strongly staining population of leukocytes. Increased CXCL10 in lesions and serum is characteristic of T1R. CXCL10 measurement offers new possibilities for laboratory diagnosis and monitoring of T1R. Studies of the regulation of CXCL10 may provide insight into the mechanisms of T1R and identify potential new drug targets for treatment.
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Chai, Qingqing, Ruiping She, Ying Huang, and Zhen F. Fu. "Expression of Neuronal CXCL10 Induced by Rabies Virus Infection Initiates Infiltration of Inflammatory Cells, Production of Chemokines and Cytokines, and Enhancement of Blood-Brain Barrier Permeability." Journal of Virology 89, no. 1 (October 22, 2014): 870–76. http://dx.doi.org/10.1128/jvi.02154-14.

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It has been shown that enhancement of blood-brain barrier (BBB) permeability is modulated by the expression of chemokines/cytokines and reduction of tight junction (TJ) proteins in the brains of mice infected with rabies virus (RABV). Since CXCL10 was found to be the most highly expressed chemokine, its temporal and spatial expression were determined in the present study. The expression of the chemokine CXCL10 was initially detected in neurons as early as 3 days postinfection (p.i.) in the brains of RABV-infected mice, after which it was detected in microglia (6 days p.i.) and astrocytes (9 days p.i.). Neutralization of CXCL10 by treatment with anti-CXCL10 antibodies reduced gamma interferon (IFN-γ) production and Th17 cell infiltration, as well as restoring TJ protein expression and BBB integrity. Together, these data suggest that it is the neuronal CXCL10 that initiates the cascade that leads to the activation of microglia/astrocytes, infiltration of inflammatory cells, expression of chemokines/cytokines, reduction of TJ protein expression, and enhancement of the BBB permeability.
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Svensson, Mattias, Soombul Zubairi, Asher Maroof, Fatima Kazi, Masaru Taniguchi, and Paul M. Kaye. "Invariant NKT Cells Are Essential for the Regulation of Hepatic CXCL10 Gene Expression during Leishmania donovani Infection." Infection and Immunity 73, no. 11 (November 2005): 7541–47. http://dx.doi.org/10.1128/iai.73.11.7541-7547.2005.

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ABSTRACT Gamma interferon (IFN-γ)-regulated chemokines of the CXC family have been implicated as key regulators of a variety of T-cell-dependent inflammatory processes. However, the cellular source(s) of IFN-γ that regulates their early expression has rarely been defined. Here, we have directly addressed this question in mice after Leishmania donovani infection. Comparison of CXCL10 mRNA accumulation in normal and IFN-γ-deficient mice confirmed an absolute requirement for IFN-γ for sustained (24 h) expression of CXCL10 mRNA accumulation in this model. In normal mice, IFN-γ was produced by both CD3int NK1.1+ NKT cells and CD3− NK1.1+ NK cells, as detected by intracellular flow cytometry. Strikingly, B6.Jα281−/− mice lacking NKT cells that express the invariant Vα14Jα18 T-cell-receptor α chain, although retaining a significant population of IFN-γ-producing NK cells and NKT cells, were unable to sustain CXCL10 mRNA accumulation. These data indicate that invariant NKT cells are indispensable for the regulation of hepatic CXCL10 gene expression during L. donovani infection.
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Jauregui, Catherine E., Qian Wang, Christopher J. Wright, Hiroki Takeuchi, Silvia M. Uriarte, and Richard J. Lamont. "Suppression of T-Cell Chemokines by Porphyromonas gingivalis." Infection and Immunity 81, no. 7 (April 15, 2013): 2288–95. http://dx.doi.org/10.1128/iai.00264-13.

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ABSTRACTPorphyromonas gingivalisis a major pathogen in periodontal disease and is associated with immune dysbiosis. In this study, we found thatP. gingivalisdid not induce the expression of the T-cell chemokine IP-10 (CXCL10) from neutrophils, peripheral blood mononuclear cells (PBMCs), or gingival epithelial cells. Furthermore,P. gingivalissuppressed gamma interferon (IFN-γ)-stimulated release of IP-10, ITAC (CXCL11), and Mig (CXCL9) from epithelial cells and inhibited IP-10 secretion in a mixed infection with the otherwise stimulatoryFusobacterium nucleatum. Inhibition of chemokine expression occurred at the level of gene transcription and was associated with downregulation of interferon regulatory factor 1 (IRF-1) and decreased levels of Stat1. Ectopic expression of IRF-1 in epithelial cells relievedP. gingivalis-induced inhibition of IP-10 release. Direct contact betweenP. gingivalisand epithelial cells was not required for IP-10 inhibition. These results highlight the immune-disruptive potential ofP. gingivalis. Suppression of IP-10 and other Th1-biasing chemokines byP. gingivalismay perturb the balance of protective and destructive immunity in the periodontal tissues and facilitate the pathogenicity of oral microbial communities.
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Asensio, Valérie C., Joachim Maier, Richard Milner, Kaan Boztug, Carrie Kincaid, Maxime Moulard, Curtis Phillipson, et al. "Interferon-Independent, Human Immunodeficiency Virus Type 1 gp120-Mediated Induction of CXCL10/IP-10 Gene Expression by Astrocytes In Vivo and In Vitro." Journal of Virology 75, no. 15 (August 1, 2001): 7067–77. http://dx.doi.org/10.1128/jvi.75.15.7067-7077.2001.

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ABSTRACT The CXC chemokine gamma interferon (IFN-γ)-inducible protein CXCL10/IP-10 is markedly elevated in cerebrospinal fluid and brain of individuals infected with human immunodeficiency virus type 1 (HIV-1) and is implicated in the pathogenesis of HIV-associated dementia (HAD). To explore the possible role of CXCL10/IP-10 in HAD, we examined the expression of this and other chemokines in the central nervous system (CNS) of transgenic mice with astrocyte-targeted expression of HIV gp120 under the control of the glial fibrillary acidic protein (GFAP) promoter, a murine model for HIV-1 encephalopathy. Compared with wild-type controls, CNS expression of the CC chemokine gene CCL2/MCP-1 and the CXC chemokine genes CXCL10/IP-10 and CXCL9/Mig was induced in the GFAP-HIV gp120 mice. CXCL10/IP-10 RNA expression was increased most and overlapped the expression of the transgene-encoded HIV gp120 gene. Astrocytes and to a lesser extent microglia were identified as the major cellular sites for CXCL10/IP-10 gene expression. There was no detectable expression of any class of IFN or their responsive genes. In astrocyte cultures, soluble recombinant HIV gp120 protein was capable of directly inducing CXCL10/IP-10 gene expression a process that was independent of STAT1. These findings highlight a novel IFN- and STAT1-independent mechanism for the regulation of CXCL10/IP-10 expression and directly link expression of HIV gp120 to the induction of CXCL10/IP-10 that is found in HIV infection of the CNS. Finally, one function of IP-10 expression may be the recruitment of leukocytes to the CNS, since the brain of GFAP-HIV gp120 mice had increased numbers of CD3+ T cells that were found in close proximity to sites of CXCL10/IP-10 RNA expression.
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Dissertations / Theses on the topic "Interferon Gamma CXCL10"

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Allen, Frederick Jr. "CCL3 Augments Antitumor Responses in CT26 by Enhancing Cellular Trafficking and Interferon-Gamma Expression." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1513124234665339.

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LOCATELLI, LUIGI. "Expression of aVB6 integrin by Pkhd1-defective cholangiocytes links enhanced ductal secretion of Macrophage chemokines to progressive portal fibrosis in Congenital Hepatic Fibrosis." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/41733.

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BACKGROUND AND AIMS: Congenital Hepatic Fibrosis (CHF) is caused by mutations in PKHD1, a gene encoding for fibrocystin, a protein of unknown function, expressed in cholangiocyte cilia and centromers. In CHF, biliary dysgenesis is accompanied by severe progressive portal fibrosis and portal hypertension. The mechanisms responsible for portal fibrosis in CHF are unclear. The αvβ6 integrin mediates local activation of TGFβ1 and is expressed by reactive cholangiocytes during cholestasis. To understand the mechanisms of fibrosis in CHF we studied the expression of αvβ6 integrin and its regulation in Pkhd1del4/del4 mice. METHODS: In Pkhd1del4/del4 mice we studied, at different ages (1-12 months): a) portal fibrosis (Sirius Red) and portal hypertension (spleen weight/body weight); b) αvβ6 mRNA and protein expression (RT-PCR, IHC); c) α-SMA and TGFβ1 mRNA expression (RT-PCR); d) portal inflammatory infiltrate (IHC for CD45 and FACS analysis of whole liver infiltrate); f) cytokines secretion from cultured monolayers of primary cholangiocytes (Luminex assay); g) cytokine effects on monocyte/macrophage proliferation (MTS assay) and migration (Boyden chamber); h) TGFβ1 and TNFα effects on β6 integrin mRNA expression by cultured cholangiocytes before and after inhibition of the TGFβ receptor type II (TGFβRII); i) TGFβ1 effects on collagen type I (COLL1) mRNA expression by cultured cholangiocytes. RESULTS: Pkhd1del4/del4 mice showed a progressive increase in αvβ6 integrin expression on biliary cyst epithelia. Expression of αvβ6 correlated with portal fibrosis (r=0.94, p<0.02) and with enrichment of a CD45+ve cell infiltrate in the portal space (r=0.97, p<0.01). Gene expression of TGFβ1 showed a similar age-dependent increase. FACS analysis showed that 50-75% of the CD45+ve cells were macrophages (CD45/CD11b/F4/80+ve). Cultured polarized Pkhd1del4/del4 cholangiocytes secreted from the basolateral side significantly increased amounts of CXCL1 and CXCL10 (p<0.05). Both cytokines were able to stimulate macrophage migration (p<0.05). Basal expression of β6 mRNA by cultured Pkhd1del4/del4 cholangiocytes (0.015±0.002 2^-dCt) was potently stimulated by the macrophage-derived cytokines TGFβ1 (0.017±0.002 2^-dCt, p<0.05) and TNFα (0.018±0.003 2^-dCt, p<0.05). Inhibition of TGFβRII completely blunted TGFβ1 (0.014±0.003 2^-dCt, p<0.05) but not TNFα effects (0.017±0.001 2^-dCt, p=ns) on β6 mRNA. COLL1 mRNA expression by cultured Pkhd1del4/del4 cholangiocytes (0.0009±0.0003 2^-dCt) was further and significantly increased after TGFβ1 stimulation (0.002±0.0005 2^-dCt, p<0.05). CONCLUSIONS: Pkhd1del4/del4 cholangiocytes possess increased basolateral secretory functions of chemokines (CXCL1, CXCL10) able to orchestrate macrophage homing to the peribiliary microenvironment. In turn, by releasing TGFβ1 and TNFα, macrophages up-regulate αvβ6 integrin in Pkhd1del4/del4 cholangiocytes. αvβ6 integrin activates latent TGFβ1, further increasing the fibrogenic properties of cholangiocytes.
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VIEIRA, DANIEL P. "Avaliação dos efeitos da inibição de cadeias imflamatórias e da suplementação exógena de CXCL 12 na hematopoiese de modelos experimentais expostos a doses letais ou subletais de radiação gama." reponame:Repositório Institucional do IPEN, 2007. http://repositorio.ipen.br:8080/xmlui/handle/123456789/11618.

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Tese (Doutoramento)
IPEN/T
Instituto de Pesquisas Energéticas e Nucleares - IPEN-CNEN/SP
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Huang, Mei-Liang, and 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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Heinz, Torsten Joseph. "Immunreaktionen im zentralen Nervensystem bei Stimulation mit Bestandteilen von Borrelia burgdorferi." Doctoral thesis, 2014. http://hdl.handle.net/11858/00-1735-0000-0022-60A8-B.

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Conference papers on the topic "Interferon Gamma CXCL10"

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Kernder, Anna, Johanna Mucke, Long Tang-Chieu, Torsten Lowin, Tim Claßen, Oliver Sander, Ellen Bleck, et al. "AB0125 CXCL17 IN RHEUMATOID ARTHRITIS: INTERFERONE-GAMMA INDUCIBLE EXPRESSION AND INHIBITION OF ANGIOGENESIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.6571.

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