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Blood, 15 April 2006, Vol. 107, No. 8, pp. 3034-3044.
Prepublished online as a Blood First Edition Paper on January 5, 2006; DOI 10.1182/blood-2005-09-3679.


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Submitted September 15, 2005
Accepted December 5, 2005

Infection-associated lymphomas derived from marginal-zone B-cells: a model of antigen-driven lymphoproliferations

Felipe Suarez, Olivier Lortholary, Olivier Hermine, and Marc Lecuit*

Department of Hematology, Necker-Enfants Malades Hospital, Paris, France
Department of Infectious Diseases, Necker-Enfants Malades Hospital, Paris, France; Molecular Mycology Unit, CNRS FRE 2849, Institut Pasteur, Paris, France
Department of Hematology, Necker-Enfants Malades Hospital, Paris, France; CNRS UMR 8603, IFR94, Rene Descartes-Paris 5 University, Paris, France
Department of Infectious Diseases, Necker-Enfants Malades Hospital, Paris, France; Bacteria-Cell Interactions Unit, INSERM U604, Institut Pasteur, Paris, France

* Corresponding author; email: mlecuit{at}pasteur.fr.

Non-Hodgkin lymphomas develop from nodal and extranodal lymphoid tissues. A distinct subset of extranodal lymphomas arising from B-cells of the marginal zone (MZ) of mucosa-associated lymphoid tissue (MALT) or spleen has been individualized. Growing evidence indicates that MZ lymphomas are associated with chronic antigenic stimulation by microbial pathogens and/or autoantigens. Molecular investigations have allowed the lengthening of the list of microbial species associated with MZ lymphoproliferations, which now comprises at least five distinct members: H. pylori, C. jejuni, B. burgdorferi, C. psittaci, and HCV. A pathophysiological scenario involving chronic and sustained stimulation of the immune system leading to lymphoid transformation has emerged. It defines a distinct category of infection-associated lymphoid malignancies, in which the infectious agent does not directly infect nor transform lymphoid cells, as do the lymphotropic oncogenic viruses EBV, HHV8 and HTLV1, but rather indirectly increases the probability of lymphoid transformation by chronically stimulating the immune system to maintain a protracted proliferative state.


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