B lymphocytes and Epstein-Barr virus: The lesson of post-transplant lymphoproliferative disorders

Research output: Contribution to journalArticle

54 Citations (Scopus)

Abstract

Epstein-Barr virus (EBV) is a ubiquitous human γ-herpes virus that establishes a life-long asymptomatic infection in immunocompetent hosts by colonizing memory B lymphocytes and hijacking cellular signaling pathways that regulate antigen-dependent B-cell activation and differentiation. In patients with solid organ or hematopoietic stem cell transplantation, the defect in EBV-specific immune responses may allow the outgrowth of EBV-carrying B lymphocytes that may give rise to a spectrum of different clinico-pathologic entities encompassed by the term post-transplantation lymphoproliferative disorders (PTLD). EBV-driven immortalization of B-cells is mediated by the cooperative activity of viral proteins that derange critical cellular pathways controlling growth and/or survival of B lymphocytes. Full transformation of infected B-cells is achieved by the contribution of poorly defined additional co-factors, including microenvironmental stimuli, genetic and epigenetic alterations. The quantification of circulating EBV DNA and EBV-specific T cells are valuable tools in the clinical monitoring of EBV-associated PTLD. The recent advances in elucidation of the mechanisms underlying EBV-induced growth transformation will be instrumental in guiding the design of novel approaches for the treatment of these often life-threatening lymphoproliferative disorders.

Original languageEnglish
Pages (from-to)96-101
Number of pages6
JournalAutoimmunity Reviews
Volume7
Issue number2
DOIs
Publication statusPublished - Dec 2007

Fingerprint

Lymphoproliferative Disorders
Human Herpesvirus 4
B-Lymphocytes
Transplants
B-Lymphocyte Differentiation Antigens
CD80 Antigens
Transplantation
Asymptomatic Infections
Critical Pathways
Hematopoietic Stem Cell Transplantation
Viral Proteins
Growth
Epigenomics
Viruses
T-Lymphocytes
DNA

Keywords

  • B lymphocytes
  • Epstein-Barr virus
  • Post-transplantation lymphoproliferative disorders
  • Viral load

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

B lymphocytes and Epstein-Barr virus : The lesson of post-transplant lymphoproliferative disorders. / Dolcetti, Riccardo.

In: Autoimmunity Reviews, Vol. 7, No. 2, 12.2007, p. 96-101.

Research output: Contribution to journalArticle

@article{8b0d5c96f5e640fdbf7ffd970a5aaaa4,
title = "B lymphocytes and Epstein-Barr virus: The lesson of post-transplant lymphoproliferative disorders",
abstract = "Epstein-Barr virus (EBV) is a ubiquitous human γ-herpes virus that establishes a life-long asymptomatic infection in immunocompetent hosts by colonizing memory B lymphocytes and hijacking cellular signaling pathways that regulate antigen-dependent B-cell activation and differentiation. In patients with solid organ or hematopoietic stem cell transplantation, the defect in EBV-specific immune responses may allow the outgrowth of EBV-carrying B lymphocytes that may give rise to a spectrum of different clinico-pathologic entities encompassed by the term post-transplantation lymphoproliferative disorders (PTLD). EBV-driven immortalization of B-cells is mediated by the cooperative activity of viral proteins that derange critical cellular pathways controlling growth and/or survival of B lymphocytes. Full transformation of infected B-cells is achieved by the contribution of poorly defined additional co-factors, including microenvironmental stimuli, genetic and epigenetic alterations. The quantification of circulating EBV DNA and EBV-specific T cells are valuable tools in the clinical monitoring of EBV-associated PTLD. The recent advances in elucidation of the mechanisms underlying EBV-induced growth transformation will be instrumental in guiding the design of novel approaches for the treatment of these often life-threatening lymphoproliferative disorders.",
keywords = "B lymphocytes, Epstein-Barr virus, Post-transplantation lymphoproliferative disorders, Viral load",
author = "Riccardo Dolcetti",
year = "2007",
month = "12",
doi = "10.1016/j.autrev.2007.02.012",
language = "English",
volume = "7",
pages = "96--101",
journal = "Autoimmunity Reviews",
issn = "1568-9972",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - B lymphocytes and Epstein-Barr virus

T2 - The lesson of post-transplant lymphoproliferative disorders

AU - Dolcetti, Riccardo

PY - 2007/12

Y1 - 2007/12

N2 - Epstein-Barr virus (EBV) is a ubiquitous human γ-herpes virus that establishes a life-long asymptomatic infection in immunocompetent hosts by colonizing memory B lymphocytes and hijacking cellular signaling pathways that regulate antigen-dependent B-cell activation and differentiation. In patients with solid organ or hematopoietic stem cell transplantation, the defect in EBV-specific immune responses may allow the outgrowth of EBV-carrying B lymphocytes that may give rise to a spectrum of different clinico-pathologic entities encompassed by the term post-transplantation lymphoproliferative disorders (PTLD). EBV-driven immortalization of B-cells is mediated by the cooperative activity of viral proteins that derange critical cellular pathways controlling growth and/or survival of B lymphocytes. Full transformation of infected B-cells is achieved by the contribution of poorly defined additional co-factors, including microenvironmental stimuli, genetic and epigenetic alterations. The quantification of circulating EBV DNA and EBV-specific T cells are valuable tools in the clinical monitoring of EBV-associated PTLD. The recent advances in elucidation of the mechanisms underlying EBV-induced growth transformation will be instrumental in guiding the design of novel approaches for the treatment of these often life-threatening lymphoproliferative disorders.

AB - Epstein-Barr virus (EBV) is a ubiquitous human γ-herpes virus that establishes a life-long asymptomatic infection in immunocompetent hosts by colonizing memory B lymphocytes and hijacking cellular signaling pathways that regulate antigen-dependent B-cell activation and differentiation. In patients with solid organ or hematopoietic stem cell transplantation, the defect in EBV-specific immune responses may allow the outgrowth of EBV-carrying B lymphocytes that may give rise to a spectrum of different clinico-pathologic entities encompassed by the term post-transplantation lymphoproliferative disorders (PTLD). EBV-driven immortalization of B-cells is mediated by the cooperative activity of viral proteins that derange critical cellular pathways controlling growth and/or survival of B lymphocytes. Full transformation of infected B-cells is achieved by the contribution of poorly defined additional co-factors, including microenvironmental stimuli, genetic and epigenetic alterations. The quantification of circulating EBV DNA and EBV-specific T cells are valuable tools in the clinical monitoring of EBV-associated PTLD. The recent advances in elucidation of the mechanisms underlying EBV-induced growth transformation will be instrumental in guiding the design of novel approaches for the treatment of these often life-threatening lymphoproliferative disorders.

KW - B lymphocytes

KW - Epstein-Barr virus

KW - Post-transplantation lymphoproliferative disorders

KW - Viral load

UR - http://www.scopus.com/inward/record.url?scp=36148981135&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=36148981135&partnerID=8YFLogxK

U2 - 10.1016/j.autrev.2007.02.012

DO - 10.1016/j.autrev.2007.02.012

M3 - Article

C2 - 18035317

AN - SCOPUS:36148981135

VL - 7

SP - 96

EP - 101

JO - Autoimmunity Reviews

JF - Autoimmunity Reviews

SN - 1568-9972

IS - 2

ER -