Differential Requirements of Cellular and Humoral Immune Responses for Fv2-Associated Resistance to Erythroleukemia and for Regulation of Retrovirus-Induced Myeloid Leukemia Development
| Autor: | Hiroyuki Kawabata, Hideaki Matsukuma, Masaaki Miyazawa, Saori Kinoshita, Tomomi Chikaishi, Sachiyo Tsuji-Kawahara, Yuri Kawasaki, Mayumi Sakamoto |
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| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
Male
Mice 129 Strain T-Lymphocytes Immunology Spleen Microbiology Virus Rodent Diseases Mice Retrovirus Immune system Virology hemic and lymphatic diseases medicine Animals Humans Exertion Spleen Focus-Forming Viruses Disease Resistance B-Lymphocytes Immunity Cellular Mice Inbred BALB C biology Friend virus Myeloid leukemia biology.organism_classification Friend murine leukemia virus Immunity Humoral Mice Inbred C57BL medicine.anatomical_structure Insect Science Disease Progression Pathogenesis and Immunity Female Leukemia Erythroblastic Acute CD8 |
| Popis: | To assess the possible contribution of host immune responses to the exertion of Fv2 -associated resistance to Friend virus (FV)-induced disease development, we inoculated C57BL/6 (B6) mice that lacked various subsets of lymphocytes with FV containing no lactate dehydrogenase-elevating virus. Fv2 r B6 mice lacking CD4 + T cells developed early polycythemia and fatal erythroleukemia, while B6 mice lacking CD8 + T cells remained resistant. Erythroid progenitor cells infected with spleen focus-forming virus (SFFV) were eliminated, and no polycythemia was observed in B cell-deficient B6 mice, but they later developed myeloid leukemia associated with oligoclonal integration of ecotropic Friend murine leukemia virus. Additional depletion of natural killer and/or CD8 + T cells from B cell-deficient B6 mice resulted in the expansion of SFFV proviruses and the development of polycythemia, indicating that SFFV-infected erythroid cells are not only restricted in their growth but are actively eliminated in Fv2 r mice through cellular immune responses. |
| Databáze: | OpenAIRE |
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