Host Immune Responses in the Course of Bovine Leukemia Virus Infection.
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- KABEYA Hidenori
- Laboratory of Veterinary Public Health, Department of Veterinary Medicine, College of Bioresource Science, Nihon University
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- OHASHI Kazuhiko
- Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University
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- ONUMA Misao
- Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University
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Abstract
Bovine leukemia virus (BLV) is a type C retrovirus infecting bovine B cells and causing enzootic bovine leukosis. Since it takes long periods to develop the disease, it is believed that BLV and host immune responses are closely related. In this review, the accumulated data showing close relationship between BLV and host immune responses are summarized in 4 sections. First, we discuss the role of cell-mediated immunity in protecting hosts from BLV infection. Second, several reports showing the relationship between the disease progression and the change of cytokine profiles are summarized. In the third section, we have focused on tumor necrosis factor α (TNFα) and its two types of receptors, and the possible involvement of TNF α in the BLV-induced leukemogenesis is discussed. The expression of TNF α has been shown to be regulated by major histocompatibility complex (MHC) haplotype. The resistance to BLV infection is supposed to be established by some innate factors, which are closely related to MHC haplotype. Finally, we propose that a breeding strategy based on the MHC haplotype could be a good approach to control BLV infection. This review includes some recent data from us and other groups.
Journal
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- Journal of Veterinary Medical Science
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Journal of Veterinary Medical Science 63 (7), 703-708, 2001
JAPANESE SOCIETY OF VETERINARY SCIENCE
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Keywords
Details 詳細情報について
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- CRID
- 1390001206426217216
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- NII Article ID
- 110003920681
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- NII Book ID
- AA10796138
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- COI
- 1:CAS:528:DC%2BD3MXmtFeltbs%3D
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- ISSN
- 13477439
- 09167250
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- NDL BIB ID
- 5855911
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- PubMed
- 11503896
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- Text Lang
- en
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- Data Source
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- Abstract License Flag
- Disallowed