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dc.contributor.authorKim, Sung-Kwon
dc.contributor.authorBrehm, Michael A.
dc.contributor.authorWelsh, Raymond M.
dc.contributor.authorSelin, Liisa K.
dc.date2022-08-11T08:09:31.000
dc.date.accessioned2022-08-23T16:34:03Z
dc.date.available2022-08-23T16:34:03Z
dc.date.issued2002-06-22
dc.date.submitted2009-03-10
dc.identifier.citation<p>J Immunol. 2002 Jul 1;169(1):90-8.</p>
dc.identifier.issn0022-1767 (Print)
dc.identifier.doi10.4049/jimmunol.169.1.90
dc.identifier.pmid12077233
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38244
dc.description.abstractBy examining adoptively transferred CSFE-labeled lymphocytic choriomeningitis virus (LCMV)-immune donor T cells in Thy-1 congenic hosts inoculated with viruses or with the cytokine inducer poly(I:C), strikingly different responses of bona fide memory T cells were found in response to different stimuli. Poly(I:C) (cytokine) stimulation caused a limited synchronized division of memory CD8 T cells specific to each of five LCMV epitopes, with no increase and sometimes a loss in number, and no change in their epitope hierarchy. Homologous LCMV infection caused more than seven divisions of T cells specific for each epitope, with dramatic increases in number and minor changes in hierarchy. Infections with the heterologous viruses Pichinde and vaccinia (VV) caused more than seven divisions and increases in number of T cells specific to some putatively cross-reactive but not other epitopes and resulted in substantial changes in the hierarchy of the LCMV-specific T cells. Hence, there can be memory T cell division without proliferation (i.e., increase in cell number) in the absence of Ag and division with proliferation in the presence of Ag from homologous or heterologous viruses. Heterologous protective immunity between viruses is not necessarily reciprocal, given that LCMV protects against VV but VV does not protect against LCMV. VV elicited proliferation of LCMV-induced CD8 and CD4 T cells, whereas LCMV did not elicit proliferation of VV-induced T cells. Thus, depending on the pathogen and the sequence of infection, a heterologous agent may selectively stimulate the memory pool in patterns consistent with heterologous immunity.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=12077233&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.4049/jimmunol.169.1.90
dc.subjectAdoptive Transfer
dc.subjectAnimals
dc.subjectArenaviridae Infections
dc.subjectBystander Effect
dc.subjectCD8-Positive T-Lymphocytes
dc.subjectCell Cycle
dc.subjectCell Division
dc.subjectCell Line
dc.subjectCricetinae
dc.subjectEpitopes, T-Lymphocyte
dc.subjectFluoresceins
dc.subjectFluorescent Dyes
dc.subject*Immunologic Memory
dc.subjectLymphocyte Activation
dc.subjectLymphocyte Count
dc.subjectLymphocytic Choriomeningitis
dc.subjectcontrol
dc.subjectLymphocytic choriomeningitis virus
dc.subjectMale
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectPichinde virus
dc.subjectPoly I-C
dc.subjectSuccinimides
dc.subjectT-Lymphocyte Subsets
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleDynamics of memory T cell proliferation under conditions of heterologous immunity and bystander stimulation
dc.typeJournal Article
dc.source.journaltitleJournal of immunology (Baltimore, Md. : 1950)
dc.source.volume169
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1119
dc.identifier.contextkey770097
html.description.abstract<p>By examining adoptively transferred CSFE-labeled lymphocytic choriomeningitis virus (LCMV)-immune donor T cells in Thy-1 congenic hosts inoculated with viruses or with the cytokine inducer poly(I:C), strikingly different responses of bona fide memory T cells were found in response to different stimuli. Poly(I:C) (cytokine) stimulation caused a limited synchronized division of memory CD8 T cells specific to each of five LCMV epitopes, with no increase and sometimes a loss in number, and no change in their epitope hierarchy. Homologous LCMV infection caused more than seven divisions of T cells specific for each epitope, with dramatic increases in number and minor changes in hierarchy. Infections with the heterologous viruses Pichinde and vaccinia (VV) caused more than seven divisions and increases in number of T cells specific to some putatively cross-reactive but not other epitopes and resulted in substantial changes in the hierarchy of the LCMV-specific T cells. Hence, there can be memory T cell division without proliferation (i.e., increase in cell number) in the absence of Ag and division with proliferation in the presence of Ag from homologous or heterologous viruses. Heterologous protective immunity between viruses is not necessarily reciprocal, given that LCMV protects against VV but VV does not protect against LCMV. VV elicited proliferation of LCMV-induced CD8 and CD4 T cells, whereas LCMV did not elicit proliferation of VV-induced T cells. Thus, depending on the pathogen and the sequence of infection, a heterologous agent may selectively stimulate the memory pool in patterns consistent with heterologous immunity.</p>
dc.identifier.submissionpathoapubs/1119
dc.contributor.departmentDepartment of Pathology
dc.source.pages90-8


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