Epstein-Barr virus-dependent lymphoproliferative disease: critical role of IL-6
Details
Serval ID
serval:BIB_0D242A561BB7
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Epstein-Barr virus-dependent lymphoproliferative disease: critical role of IL-6
Journal
European Journal of Immunology
ISSN
0014-2980 (Print)
Publication state
Published
Issued date
07/2000
Volume
30
Number
7
Pages
2065-2073
Language
english
Notes
Journal Article Research Support, Non-U.S. Gov't --- Old month value: Jul
Abstract
Epstein-Barr virus (EBV)-induced lymphoproliferative disease (lpd) is a B cell neoplasm that affects patients who are immunosuppressed in the context of organ transplantation or HIV infection. A model for the aggressive form of this entity was generated by xenotransplantation of SCID mice with human peripheral blood leukocytes from individuals with prior contact with EBV. This model, where large B cell lymphoma occurs, was used to test the hypothesis that IL-6 has a major role in EBV-induced B cell tumorigenesis. IL-6 is known to differentiate B cells into immunoglobulin-secreting plasma cells and induce EBV replication, and xenochimeric animals have detectable serum levels of human IL-6. Human IL-6 inhibition with a neutralizing monoclonal antibody decreased tumor incidence from 62 % to 27 %. In addition, anti-IL-6 treatment significantly improved xenotransplanted animal survival, with median survival at > 245 days when compared to that of controls at 132 days. In conclusion, IL-6 plays a critical role in the pathogenesis of EBV-induced human lpd, and IL-6 inhibition may represent a new and promising preventive or therapeutic approach against this malignancy.
Keywords
Animals Antibodies, Viral/blood Burkitt Lymphoma/immunology Cell Transplantation Cells, Cultured Disease Models, Animal Herpesvirus 4, Human/*immunology Humans Incidence Interleukin-6/*immunology Leukocytes, Mononuclear/immunology Lymphoproliferative Disorders/*immunology Mice Mice, SCID
Pubmed
Web of science
Open Access
Yes
Create date
25/01/2008 16:27
Last modification date
20/08/2019 13:34