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dc.contributor.authorSelin, Liisa K.
dc.contributor.authorLin, Meei-Yun
dc.contributor.authorKraemer, Kristy A.
dc.contributor.authorPardoll, Drew M.
dc.contributor.authorSchneck, Jonathan P.
dc.contributor.authorVarga, Steven Michael
dc.contributor.authorSantolucito, Paul A.
dc.contributor.authorPinto, Amelia K.
dc.contributor.authorWelsh, Raymond M.
dc.date2022-08-11T08:08:48.000
dc.date.accessioned2022-08-23T16:08:44Z
dc.date.available2022-08-23T16:08:44Z
dc.date.issued2000-01-08
dc.date.submitted2008-12-10
dc.identifier.citation<p>Immunity. 1999 Dec;11(6):733-42.</p>
dc.identifier.issn1074-7613 (Print)
dc.identifier.doi10.1016/S1074-7613(00)80147-8
dc.identifier.pmid10626895
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32520
dc.description.abstractUsing a variety of techniques, including limiting dilution assays (LDA), intracellular IFNgamma assays, and Db-IgG1 MHC dimer staining to measure viral peptide-specific T cell number and function, we show here that heterologous virus infections quantitatively delete and qualitatively alter the memory pool of T cells specific to a previously encountered virus. We also show that a prior history of a virus infection can alter the hierarchy of the immunodominant peptide response to a second virus and that virus infections selectively reactivate memory T cells with distinct specificities to earlier viruses. These results are consistent with a model for the immune system that accommodates memory T cell populations for multiple pathogens over the course of a lifetime.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=10626895&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1016/S1074-7613(00)80147-8
dc.subjectAnimals; Antigens, Viral; CD8-Positive T-Lymphocytes; Cell Line, Transformed; Dimerization; Epitopes, T-Lymphocyte; H-2 Antigens; Immunodominant Epitopes; Immunoglobulin G; Immunologic Memory; Interferon Type II; Lymphocytic choriomeningitis virus; Major Histocompatibility Complex; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Muromegalovirus; Pichinde virus; Receptors, Antigen, T-Cell, alpha-beta; Staining and Labeling; Vaccinia virus; Virus Diseases
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleAttrition of T cell memory: selective loss of LCMV epitope-specific memory CD8 T cells following infections with heterologous viruses
dc.typeJournal Article
dc.source.journaltitleImmunity
dc.source.volume11
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1088
dc.identifier.contextkey679626
html.description.abstract<p>Using a variety of techniques, including limiting dilution assays (LDA), intracellular IFNgamma assays, and Db-IgG1 MHC dimer staining to measure viral peptide-specific T cell number and function, we show here that heterologous virus infections quantitatively delete and qualitatively alter the memory pool of T cells specific to a previously encountered virus. We also show that a prior history of a virus infection can alter the hierarchy of the immunodominant peptide response to a second virus and that virus infections selectively reactivate memory T cells with distinct specificities to earlier viruses. These results are consistent with a model for the immune system that accommodates memory T cell populations for multiple pathogens over the course of a lifetime.</p>
dc.identifier.submissionpathgsbs_sp/1088
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages733-42


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