Interleukin-8 in the pathogenesis of primary central nervous system lymphoma in association with HIV infection
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- Atsushi Sasakawa
- Department of HematologyKinki University School of Medicine, Osaka, Japan
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- Chikara Hirase
- Department of HematologyKinki University School of Medicine, Osaka, Japan
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- Terufumi Yamaguchi
- Department of HematologyKinki University School of Medicine, Osaka, Japan
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- Yasuyoshi Morita
- Department of HematologyKinki University School of Medicine, Osaka, Japan
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- Jun-ichi Miyatake
- Department of HematologyKinki University School of Medicine, Osaka, Japan
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- Itaru Matsumura
- Department of HematologyKinki University School of Medicine, Osaka, Japan
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- Yasuhiro Maeda
- Department of HematologyNational Hospital Organization Osaka Minami Medical Center, Osaka, Japan
Description
The pathogenesis of acquired immunodeficiency syndrome-associated primary central nervous system lymphoma (AIDS-associated PCNSL) remains unclear. However, cell adhesion molecules have been reported to be strongly associated with PCNSL. In this study, we established Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCLs) from HIV-positive patients (LCL(HIV)) and normal individuals (LCL(N)). The expression of CD18 antigen by LCL(HIV) was stronger than that by LCL(N). We performed a cell adhesion assay using ISO-HAS, which is the human hemangiosarcoma cell line and expresses intercellular adhesion molecule 1 (CD54). The binding rates of LCL(HIV) and ISO-HAS without stimulation were higher than those of LCL(N). Further, we demonstrated that azidothymidine or simvastatin inhibited the binding rates of LCL(HIV) and ISO-HAS more significantly than those of LCL(N). Further, the levels of interleukin (IL)-8, a CD18 inducer, were higher in LCL(HIV) than in LCL(N). We conclude that interaction between IL-8 and CD18 may be critical to AIDS-related PCNSL.
Journal
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- Hematology
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Hematology 17 (3), 144-150, 2012-05
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