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Articoli di riviste sul tema "IP-10"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 3 febbraio 2022

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1

Ruffilli, I., S. Ferrari, M. Colaci, C. Ferri, P. Fallahi, and A. Antonelli. "IP-10 in Autoimmune Thyroiditis." Hormone and Metabolic Research 46, no. 09 (June 30, 2014): 597–602. http://dx.doi.org/10.1055/s-0034-1382053.

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2

Yamashita, T., H. Akamatsu, A. Tomitaka, Y. Ogawa, N. Sugawara, and K. Matsunaga. "IP-10 in atopic dermatitis." Allergy 58, no. 3 (March 2003): 261. http://dx.doi.org/10.1034/j.1398-9995.2003.00062_2.x.

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3

Bai, Xiyuan, Kathryn Chmura, Alida R. Ovrutsky, Russell P. Bowler, Robert I. Scheinman, Rebecca E. Oberley-Deegan, Haiying Liu, Shaobin Shang, Diane Ordway, and Edward D. Chan. "Mycobacterium tuberculosis increases IP-10 and MIG protein despite inhibition of IP-10 and MIG transcription." Tuberculosis 91, no. 1 (January 2011): 26–35. http://dx.doi.org/10.1016/j.tube.2010.11.005.

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4

Cornberg, Markus, and Steffen B. Wiegand. "ImPortance of IP-10 in hepatitis B." Antiviral Therapy 21, no. 2 (2015): 93–96. http://dx.doi.org/10.3851/imp3014.

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5

Nadimi, A. E. "477 IP-10 AND ACUTE MYOCARDIAL INFARCTION." Atherosclerosis Supplements 12, no. 1 (June 2011): 101–2. http://dx.doi.org/10.1016/s1567-5688(11)70478-0.

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6

Uruha, A., S. Noguchi, W. Sato, H. Nishimura, S. Mitsuhashi, T. Yamamura, and I. Nishino. "Plasma IP-10 level distinguishes inflammatory myopathy." Neuromuscular Disorders 25 (October 2015): S249. http://dx.doi.org/10.1016/j.nmd.2015.06.234.

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7

Uruha, Akinori, Satoru Noguchi, Wakiro Sato, Hiroaki Nishimura, Satomi Mitsuhashi, Takashi Yamamura, and Ichizo Nishino. "Plasma IP-10 level distinguishes inflammatory myopathy." Neurology 85, no. 3 (July 1, 2015): 293–94. http://dx.doi.org/10.1212/wnl.0000000000001767.

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8

Jabeen, Talat, Philip Leonard, Haryati Jamaluddin, and K. Ravi Acharya. "Structure of mouse IP-10, a chemokine." Acta Crystallographica Section D Biological Crystallography 64, no. 6 (May 14, 2008): 611–19. http://dx.doi.org/10.1107/s0907444908007026.

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9

Yang, Chun-Kang, Dao-Da Chen, Yuan Tian, and Jing-Hui Zhang. "Chemokine IP-10 produced by colorectal carcinoma." World Chinese Journal of Digestology 11, no. 11 (November 15, 2003): 1703–5. http://dx.doi.org/10.11569/wcjd.v11.i11.1703.

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10

TAKAKU, Y., T. KOBAYASHI, T. SOMA, K. HAGIWARA, M. KANAZAWA, and M. NAGATA. "IP-10 Induces Eosinophil Superoxide Anion Generation." Journal of Allergy and Clinical Immunology 121, no. 2 (February 2008): S46. http://dx.doi.org/10.1016/j.jaci.2007.12.186.

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11

Tebo, Julie M., Hee Sun Kim, Jing Gao, David A. Armstrong, and Thomas A. Hamilton. "Interleukin-10 Suppresses IP-10 Gene Transcription by Inhibiting the Production of Class I Interferon." Blood 92, no. 12 (December 15, 1998): 4742–49. http://dx.doi.org/10.1182/blood.v92.12.4742.

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Abstract Interleukin-10 (IL-10) selectively inhibited lipopolysaccharide (LPS)-induced chemoattractant cytokine gene expression: levels of IP-10 mRNA were markedly suppressed in IL-10–treated mouse peritoneal macrophages, whereas the expression of the RANTES mRNA was only modestly reduced. IL-10 inhibited IP-10 mRNA accumulation by reducing IP-10 gene transcription as demonstrated by nuclear run-on analysis. Interestingly, the ability of IL-10 to inhibit expression of IP-10 was dependent on the inducing stimulus; IL-10 did not suppress interferon γ (IFNγ)- or IFNβ-stimulated IP-10 transcriptio

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12

Tebo, Julie M., Hee Sun Kim, Jing Gao, David A. Armstrong, and Thomas A. Hamilton. "Interleukin-10 Suppresses IP-10 Gene Transcription by Inhibiting the Production of Class I Interferon." Blood 92, no. 12 (December 15, 1998): 4742–49. http://dx.doi.org/10.1182/blood.v92.12.4742.424k26_4742_4749.

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Interleukin-10 (IL-10) selectively inhibited lipopolysaccharide (LPS)-induced chemoattractant cytokine gene expression: levels of IP-10 mRNA were markedly suppressed in IL-10–treated mouse peritoneal macrophages, whereas the expression of the RANTES mRNA was only modestly reduced. IL-10 inhibited IP-10 mRNA accumulation by reducing IP-10 gene transcription as demonstrated by nuclear run-on analysis. Interestingly, the ability of IL-10 to inhibit expression of IP-10 was dependent on the inducing stimulus; IL-10 did not suppress interferon γ (IFNγ)- or IFNβ-stimulated IP-10 transcription or mRNA

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13

Dufour, Jennifer H., Michelle Dziejman, Michael T. Liu, Josephine H. Leung, Thomas E. Lane та Andrew D. Luster. "IFN-γ-Inducible Protein 10 (IP-10; CXCL10)-Deficient Mice Reveal a Role for IP-10 in Effector T Cell Generation and Trafficking". Journal of Immunology 168, № 7 (1 квітня 2002): 3195–204. http://dx.doi.org/10.4049/jimmunol.168.7.3195.

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14

Yates-Binder, Cecelia C., Margaret Rodgers, Jesse Jaynes, Alan Wells, Richard J. Bodnar, and Timothy Turner. "An IP-10 (CXCL10)-Derived Peptide Inhibits Angiogenesis." PLoS ONE 7, no. 7 (July 16, 2012): e40812. http://dx.doi.org/10.1371/journal.pone.0040812.

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15

Lei, Jie, Xiaowan Yin, Hong Shang, and Yongjun Jiang. "IP-10 is highly involved in HIV infection." Cytokine 115 (March 2019): 97–103. http://dx.doi.org/10.1016/j.cyto.2018.11.018.

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16

Boorsma, D. M., J. Flier, S. Sampat, C. Ottevanger, P. de Haan, L. Hooft, R. Willemze, C. P. Tensen, and T. J. Stoof. "Chemokine IP-10 expression in cultured human keratinocytes." Archives of Dermatological Research 290, no. 6 (July 8, 1998): 335–41. http://dx.doi.org/10.1007/s004030050314.

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17

Kobayashi, T., T. Soma, Y. Takaku, K. Hagiwara, M. Kanazawa, and M. Nagata. "IP-10 Augments Eosinophil Adhesion To ICAM-1." Journal of Allergy and Clinical Immunology 119, no. 1 (January 2007): S216. http://dx.doi.org/10.1016/j.jaci.2006.12.218.

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18

Kakumanu, S., W. W. Busse та J. E. Gern. "IP-10 Moderates Rhinovirus Induced IFN-α Production and Stimulates IL-10". Journal of Allergy and Clinical Immunology 119, № 1 (січень 2007): S139. http://dx.doi.org/10.1016/j.jaci.2006.11.672.

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19

Hancock, Wayne W., Wei Gao, Vilmos Csizmadia, Kerrie L. Faia, Nida Shemmeri, and Andrew D. Luster. "Donor-Derived Ip-10 Initiates Development of Acute Allograft Rejection." Journal of Experimental Medicine 193, no. 8 (April 16, 2001): 975–80. http://dx.doi.org/10.1084/jem.193.8.975.

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An allograft is often considered an immunologically inert playing field on which host leukocytes assemble and wreak havoc. However, we demonstrate that graft-specific physiologic responses to early injury initiate and promulgate destruction of vascularized grafts. Serial analysis of allografts showed that intragraft expression of the three chemokine ligands for the CXC chemo-kine receptor CXCR3 was induced in the order of interferon (IFN)-γ–inducible protein of 10 kD (IP-10, or CXCL10), IFN-inducible T cell α-chemoattractant (I-TAC; CXCL11), and then monokine induced by IFN-γ (Mig, CXCL9). Ini

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20

Yang, Jaeseok, Inho Choi, Sung Dae Kim, Eun Sil Kim, Bumrae Cho, Jae Young Kim та Curie Ahn. "Molecular characterization of cDNA encoding porcine IP-10 and induction of porcine endothelial IP-10 in response to human TNF-α". Veterinary Immunology and Immunopathology 117, № 1-2 (травень 2007): 124–28. http://dx.doi.org/10.1016/j.vetimm.2007.01.019.

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21

Arenberg, D. A., S. L. Kunkel, P. J. Polverini, S. B. Morris, M. D. Burdick, M. C. Glass, D. T. Taub, M. D. Iannettoni, R. I. Whyte, and R. M. Strieter. "Interferon-gamma-inducible protein 10 (IP-10) is an angiostatic factor that inhibits human non-small cell lung cancer (NSCLC) tumorigenesis and spontaneous metastases." Journal of Experimental Medicine 184, no. 3 (September 1, 1996): 981–92. http://dx.doi.org/10.1084/jem.184.3.981.

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The success of solid tumor growth and metastasis is dependent upon angiogenesis. Neovascularization within the tumor is regulated, in part, by a dual and opposing system of angiogenic and angiostatic factors. We now report that IP-10, a recently described angiostatic factor, as a potent angiostatic factor that regulates non-small cell lung cancer (NSCLC)-derived angiogenesis, tumor growth, and spontaneous metastasis. We initially found significantly elevated levels of IP-10 in freshly isolated human NSCLC samples of squamous cell carcinoma (SCCA). In contrast, levels of IP-10 were equivalent i

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22

Puapatanakul, Pongpratch, Sonchai Chansritrakul, Paweena Susantitaphong, Thornthun Ueaphongsukkit, Somchai Eiam-Ong, Kearkiat Praditpornsilpa, Wonngarm Kittanamongkolchai, and Yingyos Avihingsanon. "Interferon-Inducible Protein 10 and Disease Activity in Systemic Lupus Erythematosus and Lupus Nephritis: A Systematic Review and Meta-Analysis." International Journal of Molecular Sciences 20, no. 19 (October 8, 2019): 4954. http://dx.doi.org/10.3390/ijms20194954.

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There is increasing evidence of a correlation between interferon-inducible protein 10 (IP-10) and disease activity of systemic lupus erythematosus (SLE) and lupus nephritis (LN). We conducted a comprehensive search on IP-10 using MEDLINE, Scopus, and Cochrane electronic databases from the beginning to the end of December 2017. All studies that compared serum and/or urine IP-10 between active SLE/LN patients and any control groups were identified and included in this systematic review and meta-analysis. The mean difference (MD) of IP-10 level among active SLE and LN patients, as well as the cor

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23

Xu, Wei, HyeMee Joo, Sandra Clayton, Melissa Dullaers, Marie-Cecile Herve, Derek Blankenship, Maria Teresa De La Morena, et al. "Macrophages induce differentiation of plasma cells through CXCL10/IP-10." Journal of Experimental Medicine 209, no. 10 (September 17, 2012): 1813–23. http://dx.doi.org/10.1084/jem.20112142.

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In tonsils, CD138+ plasma cells (PCs) are surrounded by CD163+ resident macrophages (Mϕs). We show here that human Mϕs (isolated from tonsils or generated from monocytes in vitro) drive activated B cells to differentiate into CD138+CD38++ PCs through secreted CXCL10/IP-10 and VCAM-1 contact. IP-10 production by Mϕs is induced by B cell–derived IL-6 and depends on STAT3 phosphorylation. Furthermore, IP-10 amplifies the production of IL-6 by B cells, which sustains the STAT3 signals that lead to PC differentiation. IP-10–deficient mice challenged with NP-Ficoll show a decreased frequency of NP-s

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24

Angiolillo, A. L., C. Sgadari, D. D. Taub, F. Liao, J. M. Farber, S. Maheshwari, H. K. Kleinman, G. H. Reaman, and G. Tosato. "Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo." Journal of Experimental Medicine 182, no. 1 (July 1, 1995): 155–62. http://dx.doi.org/10.1084/jem.182.1.155.

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Human interferon-inducible protein 10 (IP-10), a member of the alpha chemokine family, inhibits bone marrow colony formation, has antitumor activity in vivo, is chemoattractant for human monocytes and T cells, and promotes T cell adhesion to endothelial cells. Here we report that IP-10 is a potent inhibitor of angiogenesis in vivo. IP-10 profoundly inhibited basic fibroblast growth factor-induced neovascularization of Matrigel (prepared by H. K. Kleinman) injected subcutaneously into athymic mice. In addition, IP-10, in a dose-dependent fashion, suppressed endothelial cell differentiation into

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25

Min, Fangui, Ruike Wu, Jinchun Pan, Shuwu Huang, Yinzhu Luo та Yu Zhang. "Positive Correlation between IP-10 and IFN-γLevels in Rhesus Monkeys(Macaca mulatta)with Either Naturally Acquired or Experimental Infection ofMycobacterium tuberculosis". BioMed Research International 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/5089752.

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Numerous studies identify that IP-10 and IFN-γare involved in leucocyte migration and activation and regarded as promising surrogate biomarkers in human and bovine tuberculosis infection, but there is lack of evidence for IP-10 in nonhuman primates. In this study, we directly determined IP-10 and IFN-γlevels in plasma from 30 healthy monkeys, 30 monkeys with naturally acquired tuberculosis, 4 monkeys experimentally infected with tuberculosis, and PPD stimulated whole blood of 14 monkeys with naturally acquired tuberculosis by ELISA. Higher plasma levels of IP-10 and IFN-γwere observed in natur

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26

Zhang, Weijun. "IP-10 for the diagnosis of tuberculosis in children." Medicine 98, no. 23 (June 2019): e15977. http://dx.doi.org/10.1097/md.0000000000015977.

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27

Bodnar, R. J., C. C. Yates, M. E. Rodgers, X. Du, and A. Wells. "IP-10 induces dissociation of newly formed blood vessels." Journal of Cell Science 122, no. 12 (May 26, 2009): 2064–77. http://dx.doi.org/10.1242/jcs.048793.

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28

Barrios, Yvelise, Paloma Poza-Guedes, Inmaculada Sanchez-Machín, Andres Franco, Honorio Armas, Ruperto Gonzalez, and Victor Matheu. "IP-10 In Pediatric Celiac Disease and Food Allergy." American Journal of Gastroenterology 109, no. 7 (July 2014): 1085–86. http://dx.doi.org/10.1038/ajg.2014.127.

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29

Nakaya, Izaya, Takashi Wada, Kengo Furuichi, Norihiko Sakai, Kiyoki Kitagawa, Hitoshi Yokoyama, Yuko Ishida, et al. "Blockade of IP-10/CXCR3 Promotes Progressive Renal Fibrosis." Nephron Experimental Nephrology 107, no. 1 (July 31, 2007): e12-e21. http://dx.doi.org/10.1159/000106505.

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30

Lin, Ching-Shwun, Guiting Lin, Kuo-Chiang Chen, Hao-Chung Ho, and Tom F. Lue. "Vascular Endothelial Growth Factor Induces IP-10 Chemokine Expression." Biochemical and Biophysical Research Communications 292, no. 1 (March 2002): 79–82. http://dx.doi.org/10.1006/bbrc.2002.6611.

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31

Farber, Joshua M. "Mig and IP-10: CXC chemokines that target lymphocytes." Journal of Leukocyte Biology 61, no. 3 (March 1997): 246–57. http://dx.doi.org/10.1002/jlb.61.3.246.

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32

Kakumanu, S., M. Evans, W. W. Busse, and J. E. Gern. "Infection with Rhinovirus Induces a Systemic IP-10 Response." Journal of Allergy and Clinical Immunology 117, no. 2 (February 2006): S114. http://dx.doi.org/10.1016/j.jaci.2005.12.458.

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33

Lee, Z. H., J. H. Lee, H. N. Kim, and H. Ha. "Essential role of IP-10 amplification in bone metastasis." Bone 47 (June 2010): S112. http://dx.doi.org/10.1016/j.bone.2010.04.237.

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34

Galbis-Martínez, Marisa, Luis Saenz, Pablo Ramírez, Pascual Parrilla та José Yélamos. "Poly(ADP-ribose) polymerase-1 modulates interferon-γ-inducible protein (IP)-10 expression in murine embryonic fibroblasts by stabilizing IP-10 mRNA". Molecular Immunology 47, № 7-8 (квітень 2010): 1492–99. http://dx.doi.org/10.1016/j.molimm.2010.01.022.

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35

Aresvik, D. M., K. Lima, T. Øverland, T. E. Mollnes, and T. G. Abrahamsen. "Increased Levels of Interferon-Inducible Protein 10 (IP-10) in 22q11.2 Deletion Syndrome." Scandinavian Journal of Immunology 83, no. 3 (March 2016): 188–94. http://dx.doi.org/10.1111/sji.12406.

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36

Sun, Hui, Namita Kundu, Russell Dorsey, Marion J. Jackson, and Amy M. Fulton. "Expression of the Chemokines IP-10 and Mig in IL-10 Transduced Tumors." Journal of Immunotherapy 24, no. 2 (March 2001): 138–43. http://dx.doi.org/10.1097/00002371-200103000-00008.

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37

Leavitt, Colton, Neil A. Zakai, Paul Auer, Mary Cushman, Ethan M. Lange, Emily B. Levitan, Nels Olson, et al. "Interferon gamma-induced protein 10 (IP-10) and cardiovascular disease in African Americans." PLOS ONE 15, no. 4 (April 2, 2020): e0231013. http://dx.doi.org/10.1371/journal.pone.0231013.

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38

Lauw, Fanny N., Andrew J. H. Simpson, Jan M. Prins, Sander J. H. van Deventer, Wipada Chaowagul, Nicholas J. White та Tom van der Poll. "The CXC Chemokines Gamma Interferon (IFN-γ)-Inducible Protein 10 and Monokine Induced by IFN-γ Are Released during Severe Melioidosis". Infection and Immunity 68, № 7 (1 липня 2000): 3888–93. http://dx.doi.org/10.1128/iai.68.7.3888-3893.2000.

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ABSTRACT Gamma interferon (IFN-γ)-inducible protein 10 (IP-10) and monokine induced by IFN-γ (Mig) are related CXC chemokines which bind to the CXCR3 receptor and specifically target activated T lymphocytes and natural killer (NK) cells. The production of IP-10 and Mig by various cell types in vitro is strongly dependent on IFN-γ. To determine whether IP-10 and Mig are released during bacterial infection in humans, we measured plasma levels of IP-10 and Mig in patients with melioidosis, a severe gram-negative infection caused byBurkholderia pseudomallei. IP-10 and Mig were markedly elevated in

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39

Luster, A. D., S. M. Greenberg, and P. Leder. "The IP-10 chemokine binds to a specific cell surface heparan sulfate site shared with platelet factor 4 and inhibits endothelial cell proliferation." Journal of Experimental Medicine 182, no. 1 (July 1, 1995): 219–31. http://dx.doi.org/10.1084/jem.182.1.219.

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IP-10 is a member of the chemokine family of cytokines and is induced in a variety of cells in response to interferon gamma and lipopolysaccharide. The self-aggregation common to many chemokines, including IP-10, has hindered the identification of a specific IP-10 receptor. Using an IP-10 alkaline phosphatase fusion protein that fortuitously blocks this self-aggregation, we have identified an IP-10 binding site on a variety of cells including endothelial, epithelial, and hematopoietic cells. This binding site has a Kd of 25 nM, is inhibited by recombinant murine or human IP-10, and is dependen

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40

Gottlieb, A. B., A. D. Luster, D. N. Posnett, and D. M. Carter. "Detection of a gamma interferon-induced protein IP-10 in psoriatic plaques." Journal of Experimental Medicine 168, no. 3 (September 1, 1988): 941–48. http://dx.doi.org/10.1084/jem.168.3.941.

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The pathologic features of psoriatic plaques are inflammation and increased epidermal turnover. IP-10, a cytokine the expression of which is induced by gamma-interferon, is a member of a family of soluble mediators with inflammatory and growth-promoting activities. IP-10 protein was detected in keratinocytes and the dermal infiltrate from active psoriatic plaques using an affinity-purified rabbit anti-IP-10 antibody in immunoperoxidase studies. Successful treatment of active plaques decreased IP-10 expression in plaques. These results were corroborated by Northern blot analysis with an IP-10 c

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41

Sgadari, C., AL Angiolillo, and G. Tosato. "Inhibition of angiogenesis by interleukin-12 is mediated by the interferon-inducible protein 10." Blood 87, no. 9 (May 1, 1996): 3877–82. http://dx.doi.org/10.1182/blood.v87.9.3877.bloodjournal8793877.

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Interleukin 12 (IL-12), a multifunctional cytokine produced by macrophages and B-cell lines, induces interferon-gamma (IFN-gamma) production, stimulates growth of both T and natural killer cells, promotes Th1-type helper T-cell responses, and inhibits neovascularization. Because the human interferon-inducible protein 10 (IP-10) can also inhibit neovascularization, we tested whether IP-10, induced by IL-12 through the intermediate IFN-gamma, might be a mediator of IL-12 angiogenesis inhibition. We report here that murine IL-12 profoundly inhibited basic fibroblast growth factor (bFGF)- induced

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42

Gattass, C. R., L. B. King, A. D. Luster, and J. D. Ashwell. "Constitutive expression of interferon gamma-inducible protein 10 in lymphoid organs and inducible expression in T cells and thymocytes." Journal of Experimental Medicine 179, no. 4 (April 1, 1994): 1373–78. http://dx.doi.org/10.1084/jem.179.4.1373.

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Abstract (sommario):

Interferon gamma-inducible protein 10 (IP-10), a member of a family of small proinflammatory chemotactic polypeptides, is expressed in interferon gamma-stimulated keratinocytes, macrophages, fibroblasts, and endothelial cells. Here we report that IP-10 is also expressed by activated but not resting T hybridoma cells, normal T cells, and thymocytes. Although resting lymphocytes did not synthesize IP-10, surprisingly high levels of IP-10 transcripts were found in lymphoid organs (spleen, thymus, and lymph nodes). Thymic and splenic stromal cells were found to express constitutively high levels o

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Taub, D. D., A. R. Lloyd, K. Conlon, J. M. Wang, J. R. Ortaldo, A. Harada, K. Matsushima, D. J. Kelvin, and J. J. Oppenheim. "Recombinant human interferon-inducible protein 10 is a chemoattractant for human monocytes and T lymphocytes and promotes T cell adhesion to endothelial cells." Journal of Experimental Medicine 177, no. 6 (June 1, 1993): 1809–14. http://dx.doi.org/10.1084/jem.177.6.1809.

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Abstract (sommario):

The human cytokine interferon-inducible protein 10 (IP-10) is a small glycoprotein secreted by activated T cells, monocytes, endothelial cells, and keratinocytes, and is structurally related to a family of chemotactic cytokines called chemokines. Although this protein is present in sites of delayed-type hypersensitivity reactions and lepromatous leprosy lesions, the biological activity of IP-10 remains unknown. We report here that recombinant human IP-10 stimulated significant in vitro chemotaxis of human peripheral blood monocytes but not neutrophils. Recombinant human IP-10 also stimulated c

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Waters, W. R., T. C. Thacker, B. J. Nonnecke, M. V. Palmer, I. Schiller, B. Oesch, H. M. Vordermeier, E. Silva та D. M. Estes. "Evaluation of Gamma Interferon (IFN-γ)-Induced Protein 10 Responses for Detection of Cattle Infected with Mycobacterium bovis: Comparisons to IFN-γ Responses". Clinical and Vaccine Immunology 19, № 3 (11 січня 2012): 346–51. http://dx.doi.org/10.1128/cvi.05657-11.

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ABSTRACTGamma interferon (IFN-γ)-induced protein 10 (IP-10) has recently shown promise as a diagnostic biomarker ofMycobacterium tuberculosisinfection of humans. The aim of the current study was to compare IP-10 and IFN-γ responses uponMycobacterium bovisinfection in cattle by using archived samples from two aerosol inoculation studies. In the first study (104CFUM. bovisby aerosol,n= 7),M. bovispurified protein derivative (PPDb)-specific IP-10 and IFN-γ gene expression was detected as early as 29 days after challenge. PPDb-specific IP-10 and IFN-γ mRNA responses followed a similar pattern of e

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Borgland, Stephanie L., Gloria P. Bowen, Norman C. W. Wong, Towia A. Libermann та Daniel A. Muruve. "Adenovirus Vector-Induced Expression of the C-X-C Chemokine IP-10 Is Mediated through Capsid-Dependent Activation of NF-κB". Journal of Virology 74, № 9 (1 травня 2000): 3941–47. http://dx.doi.org/10.1128/jvi.74.9.3941-3947.2000.

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ABSTRACT The use of adenovirus vectors for gene therapy has been limited by well-defined cellular and humoral immune responses. We have previously shown that adenovirus vectors rapidly induce the expression of the C-X-C chemokine, interferon-inducible protein 10 (IP-10), in vivo. Various first-generation, type 5 adenovirus vectors, including adCMVβgal and UV-psoralen-inactivated adenovirus, equally induced the expression of IP-10 mRNA as early as 3 h following infection in mouse renal epithelial cells (REC). Luciferase reporter experiments using deletional mutants of the murine IP-10 5′-flanki

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Shahera, Umme, Shahinul Alam, Munira Jahan, Afzalun Nessa, Saifullah Munshi, and Shahina Tabassum. "Correlation of IP-10 gene expression with Serum alanine transaminase (ALT) levels and Hepatitis B viral load in cirrhosis and hepatocellular carcinoma (HCC) patients." Bangladesh Journal of Medical Microbiology 10, no. 2 (July 28, 2016): 9–13. http://dx.doi.org/10.3329/bjmm.v10i2.51925.

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Interferon-gamma induced protein 10 (IP-10), a chemokine is suggested to be involved in liver injury during Hepatitis B virus infection (HBV). The increase of IP-10 is a critical step for recruitment of inflammatory cells to the local focus of the liver and hepatopathology. This study was designed to assess the correlation of IP-10 gene expression with HBV-DNA and serumAlanine transaminase(ALT) in patients with cirrhosis and HCC.The study was conducted among 60 patients. The study populationwere divided into four groups (15 in each groups)-HBV positive cirrhosis, HBV negative cirrhosis, HBV po

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Kawauchi, Yusuke, Kenji Suzuki, Shiro Watanabe, Satoshi Yamagiwa, Hiroyuki Yoneyama, Gi Dong Han, Suresh S. Palaniyandi, et al. "Role of IP-10/CXCL10 in the progression of pancreatitis-like injury in mice after murine retroviral infection." American Journal of Physiology-Gastrointestinal and Liver Physiology 291, no. 2 (August 2006): G345—G354. http://dx.doi.org/10.1152/ajpgi.00002.2006.

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Exocrinopathy and pancreatitis-like injury were developed in C57BL/6 (B6) mice infected with LP-BM5 murine leukemia virus, which is known to induce murine acquired immunodeficiency syndrome (MAIDS). The role of chemokines, especially CXCL10/interferon (IFN)-γ-inducible protein 10 (IP-10), a chemokine to attract CXCR3+T helper 1-type CD4+T cells, has not been investigated thoroughly in the pathogenesis of pancreatitis. B6 mice were inoculated intraperitoneally with LP-BM5 and then injected every week with either an antibody against IP-10 or a control antibody. Eight weeks after infection, we an

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Luster, A. D., and P. Leder. "IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo." Journal of Experimental Medicine 178, no. 3 (September 1, 1993): 1057–65. http://dx.doi.org/10.1084/jem.178.3.1057.

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IP-10 is a member of the -C-X-C-chemokine superfamily of proinflammatory cytokines whose secretion is induced by interferon gamma (IFN-gamma) and lipopolysaccharide (LPS). To date no function has been described for IP-10. We have genetically engineered tumor cells to secrete high levels of murine IP-10 and demonstrate that while IP-10 has no effect on the growth of these tumor cells in culture, it elicits a powerful host-mediated antitumor effect in vivo. The IP-10 antitumor response is T lymphocyte dependent, non-cell autonomous, and appears to be mediated by the recruitment of an inflammator

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Shiraha, Hidenori, Angela Glading, Kiran Gupta, and Alan Wells. "Ip-10 Inhibits Epidermal Growth Factor–Induced Motility by Decreasing Epidermal Growth Factor Receptor–Mediated Calpain Activity." Journal of Cell Biology 146, no. 1 (July 12, 1999): 243–54. http://dx.doi.org/10.1083/jcb.146.1.243.

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During wound healing, fibroblasts are recruited from the surrounding tissue to accomplish repair. The requisite migration and proliferation of the fibroblasts is promoted by growth factors including those that activate the epidermal growth factor receptor (EGFR). Counterstimulatory factors in wound fluid are postulated to limit this response; among these factors is the ELR-negative CXC chemokine, interferon inducible protein-10 (IP-10). We report here that IP-10 inhibited EGF- and heparin-binding EGF-like growth factor–induced Hs68 human dermal fibroblast motility in a dose-dependent manner (t

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Spurrell, Jason C. L., Shahina Wiehler, Raza S. Zaheer, Scherer P. Sanders, and David Proud. "Human airway epithelial cells produce IP-10 (CXCL10) in vitro and in vivo upon rhinovirus infection." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 1 (July 2005): L85—L95. http://dx.doi.org/10.1152/ajplung.00397.2004.

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Human rhinovirus (HRV) infections trigger exacerbations of asthma and chronic obstructive pulmonary disease (COPD) and are associated with lymphocytic infiltration of the airways. We demonstrate that infection of primary cultures of human airway epithelial cells, or of the BEAS-2B human bronchial epithelial cell line, with human rhinovirus type 16 (HRV-16) induces expression of CXCL10 [IFN-γ-inducible protein 10 (IP-10)], a ligand for the CXCR3 receptor found on activated type 1 T lymphocytes and natural killer cells. IP-10 mRNA reached maximal levels 24 h after HRV-16 infection then declined,

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