Show simple item record

Antigen‐specific T lymphocyte proliferation decreases over time in advanced chronic hepatitis C

dc.contributor.authorMorishima, C.en_US
dc.contributor.authorDi Bisceglie, A. M.en_US
dc.contributor.authorRothman, A. L.en_US
dc.contributor.authorBonkovsky, H. L.en_US
dc.contributor.authorLindsay, K. L.en_US
dc.contributor.authorLee, W. M.en_US
dc.contributor.authorKoziel, M. J.en_US
dc.contributor.authorFontana, R. J.en_US
dc.contributor.authorKim, H.‐y.en_US
dc.contributor.authorWright, E. C.en_US
dc.date.accessioned2012-07-12T17:25:47Z
dc.date.available2013-08-01T14:04:40Zen_US
dc.date.issued2012-06en_US
dc.identifier.citationMorishima, C.; Di Bisceglie, A. M.; Rothman, A. L.; Bonkovsky, H. L.; Lindsay, K. L.; Lee, W. M.; Koziel, M. J.; Fontana, R. J.; Kim, H.‐y. ; Wright, E. C. (2012). "Antigenâ specific T lymphocyte proliferation decreases over time in advanced chronic hepatitis C." Journal of Viral Hepatitis 19(6). <http://hdl.handle.net/2027.42/92114>en_US
dc.identifier.issn1352-0504en_US
dc.identifier.issn1365-2893en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/92114
dc.publisherBlackwell Publishing Ltden_US
dc.publisherWiley Periodicals, Inc.en_US
dc.subject.otherHepatitis C Virusen_US
dc.subject.otherCirrhosisen_US
dc.subject.otherLymphoproliferationen_US
dc.subject.otherInterferon‐Alphaen_US
dc.subject.otherFibrosisen_US
dc.subject.otherT Cellen_US
dc.titleAntigen‐specific T lymphocyte proliferation decreases over time in advanced chronic hepatitis Cen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelOncology and Hematologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDivision of Gastroenterology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USAen_US
dc.contributor.affiliationotherCenter for Infectious Disease and Vaccine Research and Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USAen_US
dc.contributor.affiliationotherDivision of Virology, Department of Laboratory Medicine, University of Washington, Seattle, WA, USAen_US
dc.contributor.affiliationotherDivision of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO, USAen_US
dc.contributor.affiliationotherDepartment of Medicine, University of Connecticut Health Center, Farmington, CT, USAen_US
dc.contributor.affiliationotherCarolinas Medical Center, Charlotte, NC, USAen_US
dc.contributor.affiliationotherDivision of Gastrointestinal and Liver Diseases, Keck School of Medicine, University of Southern California, Los Angeles, CA, USAen_US
dc.contributor.affiliationotherDivision of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, TX, USAen_US
dc.contributor.affiliationotherBeth Israel Deaconess Medical Center, Boston, MA, USAen_US
dc.contributor.affiliationotherNew England Research Institutes, Watertown, MA, USAen_US
dc.contributor.affiliationotherOffice of the Director, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USAen_US
dc.identifier.pmid22571902en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/92114/1/j.1365-2893.2011.01562.x.pdf
dc.identifier.doi10.1111/j.1365-2893.2011.01562.xen_US
dc.identifier.sourceJournal of Viral Hepatitisen_US
dc.identifier.citedreferenceGallagher KM, Lauder S, Rees IW, Gallimore AM, Godkin AJ. Type I interferon (IFN alpha) acts directly on human memory CD4+ T cells altering their response to antigen. J Immunol 2009; 183 ( 5 ): 2915 – 2920.en_US
dc.identifier.citedreferenceHavenar‐Daughton C, Kolumam GA, Murali‐Krishna K. Cutting edge: the direct action of type I IFN on CD4 T cells is critical for sustaining clonal expansion in response to a viral but not a bacterial infection. J Immunol 2006; 176 ( 6 ): 3315 – 3319.en_US
dc.identifier.citedreferenceDondi E, Rogge L, Lutfalla G, Uze G, Pellegrini S. Down‐modulation of responses to type I IFN upon T cell activation. J Immunol 2003; 170 ( 2 ): 749 – 756.en_US
dc.identifier.citedreferenceMarrack P, Kappler J, Mitchell T. Type I interferons keep activated T cells alive. J Exp Med 1999; 189 ( 3 ): 521 – 530.en_US
dc.identifier.citedreferenceSpangenberg HC, Viazov S, Kersting N et al. Intrahepatic CD8+ T‐cell failure during chronic hepatitis C virus infection. Hepatology 2005; 42 ( 4 ): 828 – 837.en_US
dc.identifier.citedreferenceLee WM, Dienstag JL, Lindsay KL et al. Evolution of the HALT‐C trial: pegylated interferon as maintenance therapy for chronic hepatitis C in previous interferon nonresponders. Control Clin Trials 2004; 25 ( 5 ): 472 – 492.en_US
dc.identifier.citedreferenceDi Bisceglie AM, Shiffman ML, Everson GT et al. Prolonged therapy of advanced chronic hepatitis C with low‐dose peginterferon. N Engl J Med 2008; 359 ( 23 ): 2429 – 2441.en_US
dc.identifier.citedreferenceMorishima C, Polyak SJ, Ray R et al. Hepatitis C virus‐specific immune responses and quasi‐species variability at baseline are associated with nonresponse to antiviral therapy during advanced hepatitis C. J Infect Dis 2006; 193 ( 7 ): 931 – 940.en_US
dc.identifier.citedreferenceShiffman ML, Di Bisceglie AM, Lindsay KL et al. Peginterferon alfa‐2a and ribavirin in patients with chronic hepatitis C who have failed prior treatment. Gastroenterology 2004; 126 ( 4 ): 1015 – 1023.en_US
dc.identifier.citedreferenceWai CT, Greenson JK, Fontana RJ et al. A simple noninvasive index can predict both significant fibrosis and cirrhosis in patients with chronic hepatitis C. Hepatology 2003; 38 ( 2 ): 518 – 526.en_US
dc.identifier.citedreferenceLok AS, Ghany MG, Goodman ZD et al. Predicting cirrhosis in patients with hepatitis C based on standard laboratory tests: results of the HALT‐C cohort. Hepatology 2005; 42 ( 2 ): 282 – 292.en_US
dc.identifier.citedreferenceThomas DL, Seeff LB. Natural history of hepatitis C. Clin Liver Dis 2005; 9 ( 3 ): 383 – 398, vi.en_US
dc.identifier.citedreferenceFreeman AJ, Marinos G, French RA, Lloyd AR. Immunopathogenesis of hepatitis C virus infection. Immunol Cell Biol 2001; 79 ( 6 ): 515 – 536.en_US
dc.identifier.citedreferenceWedemeyer H, He XS, Nascimbeni M et al. Impaired effector function of hepatitis C virus‐specific CD8+ T cells in chronic hepatitis C virus infection. J Immunol 2002; 169 ( 6 ): 3447 – 3458.en_US
dc.identifier.citedreferenceTanabe Y, Nishibori T, Su L, Arduini RM, Baker DP, David M. Cutting edge: role of STAT1, STAT3, and STAT5 in IFN‐alpha beta responses in T lymphocytes. J Immunol 2005; 174 ( 2 ): 609 – 613.en_US
dc.identifier.citedreferenceCarrion JA, Martinez‐Bauer E, Crespo G et al. Antiviral therapy increases the risk of bacterial infections in HCV‐infected cirrhotic patients awaiting liver transplantation: a retrospective study. J Hepatol 2009; 50 ( 4 ): 719 – 728.en_US
dc.identifier.citedreferencePuri RK, Travis WD, Rosenberg SA. In vivo administration of interferon alpha and interleukin 2 induces proliferation of lymphoid cells in the organs of mice. Cancer Res 1990; 50 ( 17 ): 5543 – 5550.en_US
dc.identifier.citedreferenceSiu L, Foont J, Wands JR. Hepatitis C virus and alcohol. Semin Liver Dis 2009; 29 ( 2 ): 188 – 199.en_US
dc.identifier.citedreferenceSwain S, Clise‐Dwyer K, Haynes L. Homeostasis and the age‐associated defect of CD4 T cells. Semin Immunol 2005; 17 ( 5 ): 370 – 377.en_US
dc.identifier.citedreferenceAnthony DD, Post AB, Valdez H, Peterson DL, Murphy M, Heeger PS. ELISPOT analysis of hepatitis C virus protein‐specific IFN‐gamma‐producing peripheral blood lymphocytes in infected humans with and without cirrhosis. Clin Immunol 2001; 99 ( 2 ): 232 – 240.en_US
dc.identifier.citedreferenceBonacini M, Govindarajan S, Kohla M, Lai MM, Lindsay KL. Intrahepatic lymphocyte phenotypes in hepatitis C virus infection: a comparison between cirrhotic and non‐cirrhotic livers. Minerva Gastroenterol Dietol 2007; 53 ( 1 ): 1 – 7.en_US
dc.identifier.citedreferenceMcGovern BH, Golan Y, Lopez M et al. The impact of cirrhosis on CD4+ T cell counts in HIV‐seronegative patients. Clin Infect Dis 2007; 44 ( 3 ): 431 – 437.en_US
dc.identifier.citedreferenceCramp ME, Rossol S, Chokshi S, Carucci P, Williams R, Naoumov NV. Hepatitis C virus‐specific T‐cell reactivity during interferon and ribavirin treatment in chronic hepatitis C. Gastroenterology 2000; 118 ( 2 ): 346 – 355.en_US
dc.identifier.citedreferenceMissale G, Cariani E, Lamonaca V et al. Effects of interferon treatment on the antiviral T‐cell response in hepatitis C virus genotype 1b‐ and genotype 2c‐infected patients. Hepatology 1997; 26 ( 3 ): 792 – 797.en_US
dc.identifier.citedreferenceZhang ZX, Milich DR, Peterson DL et al. Interferon‐alpha treatment induces delayed CD4 proliferative responses to the hepatitis C virus nonstructural protein 3 regardless of the outcome of therapy. J Infect Dis 1997; 175 ( 6 ): 1294 – 1301.en_US
dc.identifier.citedreferenceRashkin S, Rouster S, Goodman ZD, Sherman KE. T‐helper cells and liver fibrosis in hepatitis C virus‐monoinfected patients. J Viral Hepat 2010; 17 ( 3 ): 222 – 226.en_US
dc.identifier.citedreferenceDeschenes M, Villeneuve JP. Risk factors for the development of bacterial infections in hospitalized patients with cirrhosis. Am J Gastroenterol 1999; 94 ( 8 ): 2193 – 2197.en_US
dc.identifier.citedreferenceCaly WR, Strauss E. A prospective study of bacterial infections in patients with cirrhosis. J Hepatol 1993; 18 ( 3 ): 353 – 358.en_US
dc.identifier.citedreferenceKaplan DE, Sugimoto K, Ikeda F et al. T‐cell response relative to genotype and ethnicity during antiviral therapy for chronic hepatitis C. Hepatology 2005; 41 ( 6 ): 1365 – 1375.en_US
dc.identifier.citedreferenceRahman F, Heller T, Sobao Y et al. Effects of antiviral therapy on the cellular immune response in acute hepatitis C. Hepatology 2004; 40 ( 1 ): 87 – 97.en_US
dc.identifier.citedreferenceBurton JR Jr, Klarquist J, Im K et al. Prospective analysis of effector and regulatory CD4+ T cells in chronic HCV patients undergoing combination antiviral therapy. J Hepatol 2008; 49 ( 3 ): 329 – 338.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.