Studying Epstein-Barr Virus Pathologies and Immune Surveillance by Reconstructing EBV Infection in Mice

被引：20

作者：

Yasuda, Tomoharu ^{[1
]}

Wirtz, Tristan ^{[1
]}

Zhang, Baochun ^{[2
]}

Wunderlich, Thomas ^{[3
]}

Schmidt-Supprian, Marc ^{[4
]}

Sommermann, Thomas ^{[1
]}

Rajewsky, Klaus ^{[1
]}

机构：

[1] Max Delbruck Ctr Mol Med, Immune Regulat & Canc, D-13125 Berlin, Germany

[2] Harvard Med Sch, Dana Farber Canc Inst, Boston, MA 02115 USA

[3] Max Planck Inst Neurol Res, D-50931 Cologne, Germany

[4] Max Planck Inst Biochem, D-82152 Martinsried, Germany

来源：

IMMUNITY AND TOLERANCE | 2013年 / 78卷

基金：

欧洲研究理事会;

关键词：

NF-KAPPA-B; LATENT MEMBRANE-PROTEIN-1; CELLS; TRANSFORMATION; RESPONSES; SURVIVAL; RODENT; SAP;

D O I：

10.1101/sqb.2013.78.020222

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Epstein-Barr virus (EBV) is a gamma herpes virus endemic in humans and transforming human B lymphocytes. It causes a variety of human pathologies ranging from infectious mononucleosis upon acute infection to EBV-driven B-cell lymphomas. In humans, EBV-infected cells are under powerful immune surveillance by T and NK cells. If this immune surveillance is compromised as in immunosuppressed (AIDS- or posttransplantation) patients, the virus can spread from rare, EBV-containing cells and cause life-threatening pathologies. We have found that EBV immune surveillance and lymphomagenesis can be modeled in mice by targeted expression of key EBV proteins in the B-cell lineage. As EBV does not infect mouse B cells and mice have thus not coevolved with the virus, EBV exploits basic modes of the host immune response to optimize its coexistence with the host.

引用

页码：259 / 263

页数：5

共 19 条

[1] EBV persistence in memory B cells in vivo [J].

Babcock, GJ ;

Decker, LL ;

Volk, M ;

Thorley-Lawson, DA .

IMMUNITY, 1998, 9 (03) :395-404

[2] Role of NF-κB in cell survival and transcription of latent membrane protein 1 -: Expressing or Epstein-Barr virus latency III-infected cells [J].

Cahir-McFarland, ED ;

Carter, K ;

Rosenwald, A ;

Giltnane, JM ;

Henrickson, SE ;

Staudt, LM ;

Kieff, E .

JOURNAL OF VIROLOGY, 2004, 78 (08) :4108-4119

[3] Epstein-Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals [J].

Caldwell, RG ;

Wilson, JB ;

Anderson, SJ ;

Longnecker, R .

IMMUNITY, 1998, 9 (03) :405-411

[4] SLAM Family Receptors and SAP Adaptors in Immunity [J].

Cannons, Jennifer L. ;

Tangye, Stuart G. ;

Schwartzberg, Pamela L. .

ANNUAL REVIEW OF IMMUNOLOGY, VOL 29, 2011, 29 :665-705

[5] B cell receptor signal strength determines B cell fate [J].

Casola, S ;

Otipoby, KL ;

Alimzhanov, M ;

Humme, S ;

Uyttersprot, N ;

Kutok, JL ;

Carroll, MC ;

Rajewsky, K .

NATURE IMMUNOLOGY, 2004, 5 (03) :317-327

[6] Epstein-Barr virus infection. [J].

Cohen, JI .

NEW ENGLAND JOURNAL OF MEDICINE, 2000, 343 (07) :481-492

[7] The SAP and SLAM families in immune responses and X-linked lymphoproliferative disease [J].

Pablo Engel ;

Michael J. Eck ;

Cox Terhorst .

Nature Reviews Immunology, 2003, 3 (10) :813-821

[8] Regulation of Cre recombinase activity by mutated estrogen receptor ligand-binding domains [J].

Feil, R ;

Wagner, J ;

Metzger, D ;

Chambon, P .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 237 (03) :752-757

[9] Cellular responses to viral infection in humans: Lessons from Epstein-Barr virus [J].

Hislop, Andrew D. ;

Taylor, Graham S. ;

Sauce, Delphine ;

Rickinson, Alan B. .

ANNUAL REVIEW OF IMMUNOLOGY, 2007, 25 :587-617

[10] Constitutive CD40 signaling in B cells selectively activates the noncanonical NF-κB pathway and promotes lymphomagenesis [J].

Hoemig-Hoelzel, Cornelia ;

Hojer, Caroline ;

Rastelli, Julia ;

Casola, Stefano ;

Strobl, Lothar J. ;

Mueller, Werner ;

Quintanilla-Martinez, Leticia ;

Gewies, Andreas ;

Ruland, Juergen ;

Rajewsky, Klaus ;

Zimber-Strobl, Ursula .

JOURNAL OF EXPERIMENTAL MEDICINE, 2008, 205 (06) :1317-1329

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