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dc.contributor.authorMcNally, James M.
dc.contributor.authorZarozinski, Christopher C.
dc.contributor.authorLin, Meei Y.
dc.contributor.authorBrehm, Michael A.
dc.contributor.authorChen, Hong D.
dc.contributor.authorWelsh, Raymond M.
dc.date2022-08-11T08:09:01.000
dc.date.accessioned2022-08-23T16:15:48Z
dc.date.available2022-08-23T16:15:48Z
dc.date.issued2001-06-08
dc.date.submitted2008-11-21
dc.identifier.citationJ Virol. 2001 Jul;75(13):5965-76. <a href="http://dx.doi.org/10.1128/JVI.75.13.5965-5976.2001 ">Link to article on publisher's site</a>
dc.identifier.issn0022-538X (Print)
dc.identifier.doi10.1128/JVI.75.13.5965-5976.2001
dc.identifier.pmid11390598
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34180
dc.description.abstractExperiments designed to distinguish virus-specific from non-virus-specific T cells showed that bystander T cells underwent apoptosis and substantial attrition in the wake of a strong T-cell response. Memory CD8 T cells (CD8(+) CD44(hi)) were most affected. During acute viral infection, transgenic T cells that were clearly defined as non-virus specific decreased in number and showed an increase in apoptosis. Also, use of lymphocytic choriomeningitis virus (LCMV) carrier mice, which lack LCMV-specific T cells, showed a significant decline in non-virus-specific memory CD8 T cells that correlated to an increase in apoptosis in response to the proliferation of adoptively transferred virus-specific T cells. Attrition of T cells early during infection correlated with the alpha/beta interferon (IFN-alpha/beta) peak, and the IFN inducer poly(I:C) caused apoptosis and attrition of CD8(+) CD44(hi) T cells in normal mice but not in IFN-alpha/beta receptor-deficient mice. Apoptotic attrition of bystander T cells may make room for the antigen-specific expansion of T cells during infection and may, in part, account for the loss of T-cell memory that occurs when the host undergoes subsequent infections.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11390598&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1128/JVI.75.13.5965-5976.2001
dc.subjectAdoptive Transfer; Animals; Antigens, CD44; CD8-Positive T-Lymphocytes; Immunologic Memory; Interferon Type II; Interferon-alpha; Interferon-beta; Killer Cells, Natural; Lymphocytic Choriomeningitis; Male; Membrane Glycoproteins; Mice; Mice, Inbred C57BL; Mice, Transgenic; Perforin; Poly I-C; Pore Forming Cytotoxic Proteins; T-Lymphocytes
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleAttrition of bystander CD8 T cells during virus-induced T-cell and interferon responses
dc.typeJournal Article
dc.source.journaltitleJournal of virology
dc.source.volume75
dc.source.issue13
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/839
dc.identifier.contextkey670495
html.description.abstract<p>Experiments designed to distinguish virus-specific from non-virus-specific T cells showed that bystander T cells underwent apoptosis and substantial attrition in the wake of a strong T-cell response. Memory CD8 T cells (CD8(+) CD44(hi)) were most affected. During acute viral infection, transgenic T cells that were clearly defined as non-virus specific decreased in number and showed an increase in apoptosis. Also, use of lymphocytic choriomeningitis virus (LCMV) carrier mice, which lack LCMV-specific T cells, showed a significant decline in non-virus-specific memory CD8 T cells that correlated to an increase in apoptosis in response to the proliferation of adoptively transferred virus-specific T cells. Attrition of T cells early during infection correlated with the alpha/beta interferon (IFN-alpha/beta) peak, and the IFN inducer poly(I:C) caused apoptosis and attrition of CD8(+) CD44(hi) T cells in normal mice but not in IFN-alpha/beta receptor-deficient mice. Apoptotic attrition of bystander T cells may make room for the antigen-specific expansion of T cells during infection and may, in part, account for the loss of T-cell memory that occurs when the host undergoes subsequent infections.</p>
dc.identifier.submissionpathgsbs_sp/839
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentProgram in Immunology and Virology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages5965-76


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