Several infectious agents are established causes of non-Hodgkin’s lymphoma in humans. They include human immunodeficiency virus (HIV), Epstein-Barr virus (EBV), human herpes virus 8 (HHV-8), hepatitis C virus (HCV), and Helicobacter pylori. In addition, a causal role is suspected for hepatitis B virus (HBV), Borrelia burgdorferi, Campylobacter jejuni, and various Chlamydia species. For some of these agents, notably HIV, HHV-8, H. pylori, Chlamydia, and B. burgdorferi, the association seems specific to one or a few types of extra - nodal lymphomas, while EBV is associated with a variety of nodal and extranodal lymphomas. In the case of HCV, the risk of both nodal and extranodal lymphomas seems increased among chronically infected individuals. No data are available on HBV and risk of extranodal lymphoma. In the following sections, the epidemiological and pathogenetic evidence linking infectious agents to extra - nodal lymphoma is reviewed. Infectious agents may contribute to lymphomagenesis by two main pathogenetic mechanisms. First, a direct role is played mainly by viruses such as EBV and HHV-8, which infect target cells and express a variety of viral products that promote cell growth and survival. Additional environmental and genetic factors contribute to the malignant phenotype. The virus genome is usually present in all tumor cells. Secondly, infectious agents, mainly bacteria, may indirectly contribute to lymphomagenesis by providing a chronic antigenic stimulus that would drive the development of extranodal lymphomas along a continuum pathway, starting from the development of acquired mucosaassociated lymphoid tissue (MALT), through low-grade lymphoma, and ultimately leading to high-grade tumors. Proliferation of B cells may be dependent on the contact with infiltrating antigen-specific CD4+ helper T cells. Antigens derived from the infectious agent may be cross-reactive with self-antigens, which, in turn, may further sustain B cell growth. This model indicates that infectious agents could trigger autoimmune reactivity and emphasizes the likely relevant role of autoimmune mechanisms in the pathogenesis of some extranodal lymphomas (Figure 4.1). © 2008 by Taylor & Francis Group, LLC.
Boffetta, P., Dolcetti, R. (2008). Infectious etiopathogenesis of extranodal lymphomas. London : Informa Healthcare.
Infectious etiopathogenesis of extranodal lymphomas
Boffetta, P.;
2008
Abstract
Several infectious agents are established causes of non-Hodgkin’s lymphoma in humans. They include human immunodeficiency virus (HIV), Epstein-Barr virus (EBV), human herpes virus 8 (HHV-8), hepatitis C virus (HCV), and Helicobacter pylori. In addition, a causal role is suspected for hepatitis B virus (HBV), Borrelia burgdorferi, Campylobacter jejuni, and various Chlamydia species. For some of these agents, notably HIV, HHV-8, H. pylori, Chlamydia, and B. burgdorferi, the association seems specific to one or a few types of extra - nodal lymphomas, while EBV is associated with a variety of nodal and extranodal lymphomas. In the case of HCV, the risk of both nodal and extranodal lymphomas seems increased among chronically infected individuals. No data are available on HBV and risk of extranodal lymphoma. In the following sections, the epidemiological and pathogenetic evidence linking infectious agents to extra - nodal lymphoma is reviewed. Infectious agents may contribute to lymphomagenesis by two main pathogenetic mechanisms. First, a direct role is played mainly by viruses such as EBV and HHV-8, which infect target cells and express a variety of viral products that promote cell growth and survival. Additional environmental and genetic factors contribute to the malignant phenotype. The virus genome is usually present in all tumor cells. Secondly, infectious agents, mainly bacteria, may indirectly contribute to lymphomagenesis by providing a chronic antigenic stimulus that would drive the development of extranodal lymphomas along a continuum pathway, starting from the development of acquired mucosaassociated lymphoid tissue (MALT), through low-grade lymphoma, and ultimately leading to high-grade tumors. Proliferation of B cells may be dependent on the contact with infiltrating antigen-specific CD4+ helper T cells. Antigens derived from the infectious agent may be cross-reactive with self-antigens, which, in turn, may further sustain B cell growth. This model indicates that infectious agents could trigger autoimmune reactivity and emphasizes the likely relevant role of autoimmune mechanisms in the pathogenesis of some extranodal lymphomas (Figure 4.1). © 2008 by Taylor & Francis Group, LLC.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
