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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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Infection-associated lymphomas derived from marginal zone B cells: a model of antigen-driven lymphoproliferation
Felipe Suarez,
Olivier Lortholary,
Olivier Hermine, and
Marc Lecuit
From the Department of Hematology and the Department of Infectious Diseases, Assistance Publique des Hôpitaux de Paris (AP-HP) Necker-Enfants Malades Hospital, René Descartes–Paris 5 University Medical School, Paris, France; the Molecular Mycology Unit, Centre National de la Recherche Scientifique (CNRS) Formation de Recherche en Evolution (FRE) 2849, and Avenir group U604, Institut National de la Santé et de la Recherche Médicale (INSERM) U604, Institut Pasteur, Paris, France; and CNRS Unite Mixté de Recherche (UMR) 8603, Institut Fédératif de Recherche (IFR) 94, René Descartes–Paris 5 University Medical School, Paris, France.
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. The list of microbial species associated with MZ lymphoproliferations has grown longer with molecular investigations and now comprises at least 5 distinct members: H pylori, C jejuni, B burgdorferi, C psittaci, and hepatitis C virus (HCV), which have been associated with gastric lymphoma, immunoproliferative small intestinal disease, cutaneous lymphoma, ocular lymphoma, and spleen lymphoma, respectively. A pathophysiologic 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 and transform lymphoid cells, as do the lymphotropic oncogenic viruses Epstein-Barr virus (EBV), human herpesvirus 8 (HHV8), and human T-lymphotropic virus 1 (HTLV-1), 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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