title: A potential role of the NOD genetic background in mouse peritoneal macrophages for the development of primary effusion lymphoma.
abstract: Severe immunodeficient mice have become invaluable tools in human stem cell and tumor research. In this study, we compared the phagocytic activity of peritoneal macrophages against primary effusion lymphoma (PEL) among Rag-2/Jak3 double-deficient (Rag-2(-/-)Jak3(-/-)) mice with NOD and non-NOD (Balb/c and C57/BL6). We also evaluated lymphomatous effusion and infiltration in a PEL xenograft mouse model using these severe immunodeficient mice. In the phagocytic assay, peritoneal macrophages in the NOD background phagocytosed CFSE-labeled BCBL-1, a PEL cell line, less efficiently than those in the non-NOD background. BCBL-1 cells were successfully engrafted into both the NOD background and non-NOD background; however, the volume of ascites of the NOD background was significantly higher than that of the non-NOD background. Moreover, the organ invasion of PEL cells was suppressed in non-NOD background mice. Thus, the NOD genetic background is considered to contribute to more lymphomatous effusion and the infiltration of PEL cells than a non-NOD background. Our results showed that the NOD background allowed more lymphomatous effusion and infiltration than other backgrounds and peritoneal macrophages played a critical role in preventing the growth and infiltration of PEL cells.
authors: Division of Hematopoiesis, Center for AIDS Research, Kumamoto University, Honjo, Kumamoto, Japan.
authors: Hiroki
authors: H
authors: Goto
authors: Division of Hematopoiesis, Center for AIDS Research, Kumamoto University, Honjo, Kumamoto, Japan.
authors: Ryusho
authors: R
authors: Kariya
authors: Division of Hematopoiesis, Center for AIDS Research, Kumamoto University, Honjo, Kumamoto, Japan.
authors: Kouki
authors: K
authors: Matsuda
authors: Division of Hematopoiesis, Center for AIDS Research, Kumamoto University, Honjo, Kumamoto, Japan.
authors: Eriko
authors: E
authors: Kudo
authors: Department of Pathology, National Institute of Infectious Diseases, Toyama, Shinjuku, Tokyo, Japan.
authors: Harutaka
authors: H
authors: Katano
authors: Division of Hematopoiesis, Center for AIDS Research, Kumamoto University, Honjo, Kumamoto, Japan. Electronic address: okadas@kumamoto-u.ac.jp.
authors: Seiji
authors: S
authors: Okada
mesh_terms: D000818:Animals; D045744:Cell Line, Tumor; D005434:Flow Cytometry; D000068617:Genetic Background; D006801:Humans; D007150:Immunohistochemistry; D054685:Lymphoma, Primary Effusion / Q000473:pathology*; D017737:Macrophages, Peritoneal / Q000473:pathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D016688:Mice, Inbred NOD; D018345:Mice, Knockout; D010587:Phagocytosis / Q000502:physiology; D023041:Xenograft Model Antitumor Assays / Q000379:methods*
keywords: Immunodeficient mice; Macrophage; NOD; Primary effusion lymphoma