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Journal articles on the topic 'IP-10'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 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 transcription or mRNA accumulation. These results suggested that IL-10 might act indirectly to suppress IP-10 expression by inhibiting LPS-induced class I IFN production. This hypothesis was supported by the following observations. First, LPS-induced IP-10 mRNA expression was blocked in cells cotreated with cycloheximide. Second, IL-10 inhibited the production of IFN/β-mediated antiviral activity. Finally, the IL-10–mediated suppression of LPS-stimulated IP-10 production could be rescued by cotreatment with IFNβ.

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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 accumulation. These results suggested that IL-10 might act indirectly to suppress IP-10 expression by inhibiting LPS-induced class I IFN production. This hypothesis was supported by the following observations. First, LPS-induced IP-10 mRNA expression was blocked in cells cotreated with cycloheximide. Second, IL-10 inhibited the production of IFN/β-mediated antiviral activity. Finally, the IL-10–mediated suppression of LPS-stimulated IP-10 production could be rescued by cotreatment with IFNβ.

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13

Dufour, Jennifer H., Michelle Dziejman, Michael T. Liu, Josephine H. Leung, Thomas E. Lane, and 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, no. 7 (April 1, 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, and J. E. Gern. "IP-10 Moderates Rhinovirus Induced IFN-α Production and Stimulates IL-10." Journal of Allergy and Clinical Immunology 119, no. 1 (January 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). Initial IP-10 production was localized to endothelial cells, and only IP-10 was induced by isografting. Anti–IP-10 monoclonal antibodies prolonged allograft survival, but surprisingly, IP-10–deficient (IP-10−/−) mice acutely rejected allografts. However, though allografts from IP-10+/+ mice were rejected by day 7, hearts from IP-10−/− mice survived long term. Compared with IP-10+/+ donors, use of IP-10−/− donors reduced intragraft expression of cytokines, chemokines and their receptors, and associated leukocyte infiltration and graft injury. Hence, tissue-specific generation of a single chemokine in response to initial ischemia/reperfusion can initiate progressive graft infiltration and amplification of multiple effector pathways, and targeting of this proximal chemokine can prevent acute rejection. These data emphasize the pivotal role of donor-derived IP-10 in initiating alloresponses, with implications for tissue engineering to decrease immunogenicity, and demonstrate that chemokine redundancy may not be operative in vivo.

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20

Yang, Jaeseok, Inho Choi, Sung Dae Kim, Eun Sil Kim, Bumrae Cho, Jae Young Kim, and 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, no. 1-2 (May 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 in either normal lung tissue or adenocarcinoma specimens. The neoplastic cells in specimens of SCCA were the predominant cells that appeared to express IP-10 by immunolocalization. Neutralization of IP-10 in SCCA tumor specimens resulted in enhanced tumor-derived angiogenic activity. Using a model of human NSCLC tumorigenesis in SCID mice, we found that NSCLC tumor growth was inversely correlated with levels of plasma or tumor-associated IP-10. IP-10 in vitro functioned as neither an autocrine growth factor nor as an inhibitor of proliferation of the NSCLC cell lines. Reconstitution of intratumor IP-10 for a period of 8 wk resulted in a significant inhibition of tumor growth, tumor-associated angiogenic activity and neovascularization, and spontaneous lung metastases, whereas, neutralization of IP-10 for 10 wk augmented tumor growth. These findings support the notion that tumor-derived IP-10 is an important endogenous angiostatic factor in NSCLC.

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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 correlation of IP-10 with disease activity, were meta-analyzed using a random-effects model. From 23 eligible studies, 15 provided adequate data for meta-analysis. Serum IP-10 was significantly elevated in patients with active SLE compared to non-active SLE patients (MD 356.5 pg/mL, 95% CI 59.6 to 653.4, p = 0.019). On the other hand, the levels of serum IP-10 was not different between active LN and non-active LN. However, serum IP-10 was positively correlated with disease activity like SLE disease activity index (SLEDAI) (pooled r = 0.29, 95% CI 0.22 to 0.35, p < 0.001). Furthermore, urine IP-10 tended to be higher in patients with active LN compared to non-active LN patients but this did not reach statistical significance (MD 3.47 pg/mgCr × 100, 95% CI −0.18 to 7.12, p = 0.06). Nevertheless, urine IP-10 was positively correlated with renal SLEDAI (pooled r = 0.29, 95% CI 0.05 to 0.50, p = 0.019). In conclusion, serum and urine IP-10 levels may be useful in monitoring the disease activity of SLE and LN. Serum IP-10 was correlated with systemic disease whereas urine IP-10 was a useful biomarker for detecting active LN.

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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-specific PCs and lower titers of antibodies. Thus, our results reveal a novel dialog between Mϕs and B cells, in which IP-10 acts as a PC differentiation factor.

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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 tubular capillary structures in vitro. IP-10 had no effect on endothelial cell growth, attachment, and migration as assayed in vitro. These results document an important biological property of IP-10 and raise the possibility that IP-10 may participate in the regulation of angiogenesis during inflammation and tumorigenesis.

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25

Min, Fangui, Ruike Wu, Jinchun Pan, Shuwu Huang, Yinzhu Luo, and 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 natural tuberculosis monkeys than in healthy controls. The dynamic changes of plasma IP-10 and IFN-γin experimental infections showed consistent representation of a transient increase during the infection period. After PPD stimulation, release of IP-10 and IFN-γis significantly induced in natural tuberculosis monkeys, but the stimulation index of IP-10 was significantly lower than IFN-γ. Further analysis showed that positive correlation between IP-10 and IFN-γexisted in healthy and tuberculosis monkeys. Our findings support plasma IP-10 and IFN-γas biomarkers for monitoring ongoing inflammation of nonhuman primate tuberculosis, and IFN-γis a more valuable diagnostic biomarker.

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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, and 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, no. 7-8 (April 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, and 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, no. 7 (July 1, 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 patients with melioidosis on admission, particularly in blood culture-positive patients, and remained elevated during the 72-h study period. Levels of IP-10 and Mig showed a positive correlation with IFN-γ concentrations and also correlated with clinical outcome. In whole blood stimulated with heat-killed B. pseudomallei, neutralization of IFN-γ and tumor necrosis factor alpha (TNF-α) partly attenuated IP-10 and Mig release, while anti-interleukin-12 (IL-12) and anti-IL-18 had a synergistic effect. Stimulation with other bacteria or endotoxin also induced strong secretion of IP-10 and Mig. These data suggest that IP-10 and Mig are part of the innate immune response to bacterial infection. IP-10 and Mig may contribute to host defense in Th1-mediated host defense during infections by attracting CXCR3+ Th1 cells to the site of inflammation.

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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 dependent on the presence of cell surface heparan sulfate proteoglycans (HSPG). This conclusion is based on the findings that IP-10 binding to cells is: (a) inhibited by heparin and heparan sulfate; (b) sensitive to a 1 M NaCl wash; (c) eliminated by treatment with heparinase and trypsin; and (d) absent on mutant CHO cells that do not express cell surface HSPG. Platelet factor 4 (PF4), but not IL-8, monocyte chemoattractant protein-1, RANTES, monocyte inflammatory protein (MIP)-1 alpha, or MIP-1 beta, can compete effectively with IP-10 for binding to the cell surface. Furthermore, IP-10 shares with PF4 the ability to inhibit endothelial cell proliferation (IC50 = 150 nM). These studies demonstrate specificity in the interaction of chemokines and HSPG, and they define IP-10 and PF4 as a distinct subset of chemokines sharing an HSPG-binding site and angiostatic properties.

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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 cDNA probe. We have previously detected activated T cells and HLA-DR keratinocytes in active psoriatic plaques. Since IP-10 is detected in delayed cellular immune responses, the present study further points to the role of ongoing cellular immune responses in the pathogenesis of psoriasis.

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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 Matrigel neovascularization in vivo, and that this effect of IL- 12 was neutralized by systemic administration of antibodies to either murine IFN-gamma or IP-10. Murine IL-12 induced murine IP-10 expression in mouse splenocytes, and human IFN-gamma induced human IP-10 expression in purified human endothelial cells, suggesting that IL-12 can induce IP-10 expression in certain cells. These results document the important role of IP-10 as a mediator of angiogenesis inhibition by IL-12, and raise the possibility that IP-10 may also contribute to the antitumor effect of IL-12.

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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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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 of both IP-10 mRNA and protein, accounting for the high level of spontaneous expression in lymphoid tissue. Therefore, in addition to its role as a proinflammatory cytokine, IP-10 may participate in T cell effector function and perhaps T cell development.

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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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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 chemotaxis of stimulated, but not unstimulated, human peripheral blood T lymphocytes. Phenotypic analysis of the stimulated T cell population responsive to IP-10 demonstrated that stimulated CD4+ and CD29+ T cells migrated in response to IP-10. This resembles the biological activity of the previously described T cell chemoattractant RANTES. Using an endothelial cell adhesion assay, we demonstrated that stimulated T cells pretreated with optimal doses of IP-10 exhibited a greatly enhanced ability to bind to an interleukin 1-treated endothelial cell monolayer. These results demonstrate that the IP-10 gene encodes for an inflammatory mediator that specifically stimulates the directional migration of T cells and monocytes as well as potentiates T cell adhesion to endothelium.

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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, and 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, no. 3 (January 11, 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 expression over the course of this study and were highly correlated (r= 0.87). In the second study (105CFUM. bovisby aerosol,n= 5), IP-10 and IFN-γ (protein) responses to mycobacterial antigens were compared following challenge. IFN-γ responses to mycobacterial antigens were detected at 29 days after challenge and were sustained during the remainder of the study. IFN-γ responses to mycobacterial antigens exceeded corresponding responses in nonstimulated cultures. IP-10 responses to mycobacterial antigens exceeded preinfection responses at 7, 29, and 63 days after challenge. In contrast to IFN-γ responses, IP-10 responses to mycobacterial antigens generally did not exceed the respective responses in nonstimulated cultures. IP-10 responses to medium alone and to mycobacterial antigens followed a similar pattern of response. Correlations between IP-10 and IFN-γ (protein) responses were modest (r≈ 0.50 to 0.65). Taken together, these findings do not support the use of IP-10 protein as a biomarker for bovine tuberculosis using the current testing protocol and reagents; however, mRNA-based assays may be considered for further analysis.

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Borgland, Stephanie L., Gloria P. Bowen, Norman C. W. Wong, Towia A. Libermann, and 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, no. 9 (May 1, 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′-flanking region revealed that transcriptional activation of the IP-10 promoter by adCMVβgal was dependent on the −161- to −96-bp region upstream of the transcription start site. In electrophoretic mobility shift assays, adCMVβgal, adCMV-GFP, FG140, and transcription-defective adenovirus induced protein binding to oligonucleotides containing a consensus sequence for NF-κB at position −113 of the IP-10 promoter. Supershift assays confirmed an increase in binding activity of NF-κB p65 but not p50 or cRel in REC cells infected with various replication-deficient adenoviruses. Coinfection of REC cells with adCMVβgal and an adenoviral vector expressing IκBα resulted in suppression of adCMVβgal-induced expression of IP-10 at 6 and 16 h, further strengthening the conclusion that adenovirus-induced activation of IP-10 is dependent on NF-κB. The induction of IP-10 appeared to be direct because infection with adenovirus vectors failed to induce the expression of the potent IP-10 stimulators, interferon gamma and tumor necrosis factor alpha. Together, these findings demonstrate that adenovirus vectors directly induce the expression of IP-10 through capsid dependent activation of NF-κB.

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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 positiveHCC and HBV negative HCC. Expression of IP-10 gene was observed using real time PCR.IP-10 gene expressions in the above mentioned groups were correlated with serum ALT level and HBV viral load.IP-10 gene was significantly higher in HBV-positive patients with HCC than HBVpositive cirrhosis. Similarly, the expression of IP-10 was significantly higher in HBV-positive HCC than HBVnegative HCC patients. However, the expression of IP-10 was reduced in HBV-positive cirrhosis in comparison with HBV-negative cirrhosis.IP-10 gene expression in liver was not correlated with the serum levels of ALT in any of the study groups. HBV- DNA load also did not correlated with IP-10 gene expression in HBV positive HCC and HBV positive cirrhosis patients.This study shows that there was no significant change with the expression of IP-10 gene in any of the study groups with ALT level or viral load, though differential expression of IP-10 gene were observed in cirrhosis and HCC patients. Bangladesh J Med Microbiol 2016; 10 (2): 9-13

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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 analyzed the effect of IP-10 neutralization. Anti-IP-10 antibody treatment did not change the generalized lymphadenopathy and hepatosplenomegaly of mice with MAIDS. The treatment significantly reduced the number of IP-10- and CXCR3-positive cells in the mesenteric lymph nodes (mLNs) but not the phenotypes and gross numbers of cells. In contrast, IP-10 neutralization reduced the number of mononuclear cells infiltrating into the pancreas. Anti-IP-10 antibody treatment did not change the numbers of IFN-γ+and IL10+cells in the mLN but significantly reduced their numbers, especially IFN-γ+and IL-10+CD4+T cells and IFN-γ+Mac-1+cells, in the pancreas. IP-10 neutralization ameliorated the pancreatic lesions of mice with MAIDS probably by blocking the cellular infiltration of CD4+T cells and IFN-γ+Mac-1+cells into the pancreas at least at 8 wk after infection, suggesting that IP-10 and these cells might play a key role in the development of chronic autoimmune pancreatitis.

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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 inflammatory infiltrate composed of lymphocytes, neutrophils, and monocytes. These results document an important biologic property of IP-10 and raise the possibility that some of the T cell-directed effects of IFN-gamma and LPS may be mediated by this chemokine.

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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 (to 52% and 44%, respectively, at 50 ng/ml IP-10), whereas IP-10 had no effect on either basal or EGFR-mediated mitogenesis (96 ± 15% at 50 ng/ml). These data demonstrate for the first time a counterstimulatory effect of IP-10 on a specific induced fibroblast response, EGFR-mediated motility. To define the molecular basis of this negative transmodulation of EGFR signaling, we found that IP-10 did not adversely impact receptor or immediate postreceptor signaling as determined by tyrosyl phosphorylation of EGFR and two major downstream effectors phospholipase C-γ and erk mitogen-activated protein kinases. Morphological studies suggested which biophysical steps may be affected by demonstrating that IP-10 treatment resulted in an elongated cell morphology reminiscent of failure to detach the uropod; in support of this, IP-10 pretreatment inhibited EGF-induced cell detachment. These data suggested that calpain activity may be involved. The cell permeant agent, calpain inhibitor I, limited EGF-induced motility and de-adhesion similarly to IP-10. IP-10 also prevented EGF- induced calpain activation (reduced by 71 ± 7%). That this inhibition of EGF-induced calpain activity was secondary to IP-10 initiating a cAMP-protein kinase A-calpain cascade is supported by the following evidence: (a) the cell permeant analogue 8-(4-chlorophenylthio)-cAMP (CPT-cAMP) prevented EGF-induced calpain activity and motility; (b) other ELR-negative CXC chemokines, monokine induced by IFN-γ and platelet factor 4 that also generate cAMP, inhibited EGF-induced cell migration and calpain activation; and (c) the protein kinase A inhibitor Rp-8-Br-cAMPS abrogated IP-10 inhibition of cell migration, cell detachment, and calpain activation. Our findings provide a model by which IP-10 suppresses EGF-induced cell motility by inhibiting EGF-induced detachment of the trailing edges of motile cells.

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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, whereas protein levels peaked 48 h after infection with no subsequent new synthesis. Cytosolic levels of AU-rich factor 1, a protein associated with mRNA destabilization, increased beginning 24 h after HRV-16 infection. Generation of IP-10 required virus capable of replication but was not dependent on prior induction of type 1 interferons. Transfection of synthetic double-stranded RNA into epithelial cells induced robust production of IP-10, whereas transfection of single-stranded RNA had no effect. Induction of IP-10 gene expression by HRV-16 depended upon activation of NF-κB, as well as other transcription factor recognition sequences further upstream in the IP-10 promoter. In vivo infection of human volunteers with HRV-16 strikingly increased IP-10 protein in nasal lavages during symptomatic colds. Levels of IP-10 correlated with symptom severity, viral titer, and numbers of lymphocytes in airway secretions. Thus IP-10 may play a role in the pathogenesis of HRV-induced colds and in HRV-induced exacerbations of COPD and asthma.

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