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dc.contributor.authorKemball, Christopher C.
dc.contributor.authorLee, Eun D. Han
dc.contributor.authorSzomolanyi-Tsuda, Eva
dc.contributor.authorPearson, Thomas A.
dc.contributor.authorLarsen, Christian P.
dc.contributor.authorLukacher, Aron E.
dc.date2022-08-11T08:09:31.000
dc.date.accessioned2022-08-23T16:33:54Z
dc.date.available2022-08-23T16:33:54Z
dc.date.issued2006-01-21
dc.date.submitted2009-03-10
dc.identifier.citation<p>J Immunol. 2006 Feb 1;176(3):1814-24.</p>
dc.identifier.issn0022-1767 (Print)
dc.identifier.doi10.4049/jimmunol.176.3.1814
dc.identifier.pmid16424212
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38210
dc.description.abstractThe requirement for costimulation in antiviral CD8+ T cell responses has been actively investigated for acutely resolved viral infections, but it is less defined for CD8+ T cell responses to persistent virus infection. Using mouse polyoma virus (PyV) as a model of low-level persistent virus infection, we asked whether blockade of the CD40 ligand (CD40L) and CD28 costimulatory pathways impacts the magnitude and function of the PyV-specific CD8+ T response, as well as the humoral response and viral control during acute and persistent phases of infection. Costimulation blockade or gene knockout of either CD28 or CD40L substantially dampened the magnitude of the acute CD8+ T cell response; simultaneous CD28 and CD40L blockade severely depressed the acute T cell response, altered the cell surface phenotype of PyV-specific CD8+ T cells, decreased PyV VP1-specific serum IgG titers, and resulted in an increase in viral DNA levels in multiple organs. CD28 and CD40L costimulation blockade during acute infection also diminished the memory PyV-specific CD8+ T cell response and serum IgG titer, but control of viral persistence varied between mouse strains and among organs. Interestingly, we found that CD28 and CD40L costimulation is dispensable for generating and/or maintaining PyV-specific CD8+ T cells during persistent infection; however, blockade of CD27 and CD28 costimulation in persistently infected mice caused a reduction in PyV-specific CD8+ T cells. Taken together, these data indicate that CD8+ T cells primed within the distinct microenvironments of acute vs persistent virus infection differ in their costimulation requirements.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=16424212&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.4049/jimmunol.176.3.1814
dc.subjectAcute Disease
dc.subjectAnimals
dc.subjectAntigens, CD28
dc.subjectBone Marrow Transplantation
dc.subjectCD40 Ligand
dc.subjectCD8-Positive T-Lymphocytes
dc.subjectChronic Disease
dc.subjectFemale
dc.subjectImmunity, Cellular
dc.subjectLymphocyte Activation
dc.subjectMice
dc.subjectMice, Inbred C3H
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectPolyomavirus
dc.subjectPolyomavirus Infections
dc.subjectTumor Virus Infections
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleCostimulation requirements for antiviral CD8+ T cells differ for acute and persistent phases of polyoma virus infection
dc.typeJournal Article
dc.source.journaltitleJournal of immunology (Baltimore, Md. : 1950)
dc.source.volume176
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1089
dc.identifier.contextkey770067
html.description.abstract<p>The requirement for costimulation in antiviral CD8+ T cell responses has been actively investigated for acutely resolved viral infections, but it is less defined for CD8+ T cell responses to persistent virus infection. Using mouse polyoma virus (PyV) as a model of low-level persistent virus infection, we asked whether blockade of the CD40 ligand (CD40L) and CD28 costimulatory pathways impacts the magnitude and function of the PyV-specific CD8+ T response, as well as the humoral response and viral control during acute and persistent phases of infection. Costimulation blockade or gene knockout of either CD28 or CD40L substantially dampened the magnitude of the acute CD8+ T cell response; simultaneous CD28 and CD40L blockade severely depressed the acute T cell response, altered the cell surface phenotype of PyV-specific CD8+ T cells, decreased PyV VP1-specific serum IgG titers, and resulted in an increase in viral DNA levels in multiple organs. CD28 and CD40L costimulation blockade during acute infection also diminished the memory PyV-specific CD8+ T cell response and serum IgG titer, but control of viral persistence varied between mouse strains and among organs. Interestingly, we found that CD28 and CD40L costimulation is dispensable for generating and/or maintaining PyV-specific CD8+ T cells during persistent infection; however, blockade of CD27 and CD28 costimulation in persistently infected mice caused a reduction in PyV-specific CD8+ T cells. Taken together, these data indicate that CD8+ T cells primed within the distinct microenvironments of acute vs persistent virus infection differ in their costimulation requirements.</p>
dc.identifier.submissionpathoapubs/1089
dc.contributor.departmentDepartment of Pathology
dc.source.pages1814-24


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