Journal article
Role of IFN-γ responsiveness in CD8 T cell-mediated viral clearance and demyelination in coronavirus-infected mice
Journal of Neuroimmunology, Vol.194(1-2), pp.18-26
02/2008
DOI: 10.1016/j.jneuroim.2007.10.030
PMID: 18082272
Abstract
Immunocompetent, but not RAG1−/− mice infected with MHV–JHM develop demyelination. Transferred CD8 T cell-enriched splenocytes reconstitute demyelination, and this ability is dependent on donor IFN-γ. We used IFN-γR1−/− mice to examine the target of IFN-γ in CD8 T cell-mediated demyelination. In IFN-γR1−/−RAG1−/− recipients, demyelination is decreased, but not eliminated, while viral titers are significantly increased when compared to IFN-γR1+/+RAG1−/− recipients. IFN-γR1−/− CD8 T cells retain virus-specific effector function regardless of IFN-γR1 expression. Although IFN-γR1 responsiveness is critical for maximal demyelination, increased levels of infectious virus coupled with adoptive transfer of CD8 T cells may result in myelin destruction independent of IFN-γR1 expression.
Details
- Title: Subtitle
- Role of IFN-γ responsiveness in CD8 T cell-mediated viral clearance and demyelination in coronavirus-infected mice
- Creators
- Steven P Templeton - Interdisciplinary Program in Immunology, University of Iowa, Iowa City, IA 52242, United StatesStanley Perlman - Interdisciplinary Program in Immunology, University of Iowa, Iowa City, IA 52242, United States
- Resource Type
- Journal article
- Publication Details
- Journal of Neuroimmunology, Vol.194(1-2), pp.18-26
- DOI
- 10.1016/j.jneuroim.2007.10.030
- PMID
- 18082272
- NLM abbreviation
- J Neuroimmunol
- ISSN
- 0165-5728
- eISSN
- 1872-8421
- Publisher
- Elsevier B.V
- Language
- English
- Date published
- 02/2008
- Academic Unit
- Microbiology and Immunology; Stead Family Department of Pediatrics; Iowa Neuroscience Institute; Infectious Disease (Pediatrics)
- Record Identifier
- 9983777352602771
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