Persistent expression of the full genome of hepatitis C virus in B cells induces spontaneous development of B-cell lymphomas in vivo.

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Extrahepatic manifestations of hepatitis C virus (HCV) infection have been reported in 40–70% of HCV-infected patients. B-cell non-Hodgkin’s lymphoma is a typical extrahepatic manifestation frequently associated with HCV infection. Although the HCV infection of B cells has been reported, the mechanism of disease onset remains unclear. In this study we established HCV transgenic mice that express the full HCV genome in B cells (RzCD19Cre mice) and observed a 25.0% incidence of non-Hodgkin’s diffuse large B-cell lymphomas (22.2% in males and 25.9% in females) within 600 days after birth. Expression levels of aspartate aminotransferase, alanine aminotransferase, and 32 different cytokines, chemokines and growth factors were examined. The incidence of B-cell lymphoma was significantly correlated with only the level of soluble interleukin-2 receptor ! subunit (sIL-2R!) in RzCD19Cre mouse serum. All RzCD19Cre mice with substantially elevated serum sIL-2Rα levels (>1,000 pg/mL) developed B-cell lymphomas. Moreover, compared to tissues from control animals, the B-cell lymphoma tissues of RzCD19Cre mice expressed significantly higher levels of IL-2Rα. We show that the expression of HCV in B cells promotes non-Hodgkin’s-type diffuse B-cell lymphoma, and therefore, the RzCD19Cre mouse is a powerful model to study the mechanisms related to the development of HCV-associated B-cell lymphoma.

http://bloodjournal.hematologylibrary.org/content/116/23/4926

収録刊行物

  • Blood

    Blood 116 (23), 4926-4933, 2010-12-02

    American Society of Hematology

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