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dc.contributor.authorSelin, Liisa K.
dc.contributor.authorVarga, Steven Michael
dc.contributor.authorWong, Iris C.
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.issued1998-11-06
dc.date.submitted2008-12-10
dc.identifier.citation<p>J Exp Med. 1998 Nov 2;188(9):1705-15.</p>
dc.identifier.issn0022-1007 (Print)
dc.identifier.doi10.1084/jem.188.9.1705
dc.identifier.pmid9802982
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32523
dc.description.abstractA basic principle of immunology is that prior immunity results in complete protection against a homologous agent. In this study, we show that memory T cells specific to unrelated viruses may alter the host's primary immune response to a second virus. Studies with a panel of heterologous viruses, including lymphocytic choriomeningitis (LCMV), Pichinde (PV), vaccinia (VV), and murine cytomegalo (MCMV) viruses showed that prior immunity with one of these viruses in many cases enhanced clearance of a second unrelated virus early in infection. Such protective immunity was common, but it depended on the virus sequence and was not necessarily reciprocal. Cell transfer studies showed that both CD4 and CD8 T cell populations from LCMV-immune mice were required to transfer protective immunity to naive hosts challenged with PV or VV. In the case of LCMV-immune versus naive mice challenged with VV, there was an enhanced early recruitment of memory phenotype interferon (IFN) gamma-secreting CD4(+) and CD8(+) cells into the peritoneal cavity and increased IFN-gamma levels in this initial site of virus replication. Studies with IFN-gamma receptor knockout mice confirmed a role for IFN-gamma in mediating the protective effect by LCMV-immune T cell populations when mice were challenged with VV but not PV. In some virus sequences memory cell populations, although clearing the challenge virus more rapidly, elicited enhanced IFN-gamma-dependent immunopathogenesis in the form of acute fatty necrosis. These results indicate that how a host responds to an infectious agent is a function of its history of previous infections and their influence on the memory T cell pool.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=9802982&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212518/
dc.subjectAdipose Tissue; Animals; Female; Immunization; *Immunologic Memory; Interferon Type II; Lymphocytic choriomeningitis virus; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Muromegalovirus; Necrosis; Phenotype; Pichinde virus; T-Lymphocytes; T-Lymphocytes, Cytotoxic; Vaccinia virus; Virus Diseases; Viruses
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleProtective heterologous antiviral immunity and enhanced immunopathogenesis mediated by memory T cell populations
dc.typeJournal Article
dc.source.journaltitleThe Journal of experimental medicine
dc.source.volume188
dc.source.issue9
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1090
dc.identifier.contextkey679628
html.description.abstract<p>A basic principle of immunology is that prior immunity results in complete protection against a homologous agent. In this study, we show that memory T cells specific to unrelated viruses may alter the host's primary immune response to a second virus. Studies with a panel of heterologous viruses, including lymphocytic choriomeningitis (LCMV), Pichinde (PV), vaccinia (VV), and murine cytomegalo (MCMV) viruses showed that prior immunity with one of these viruses in many cases enhanced clearance of a second unrelated virus early in infection. Such protective immunity was common, but it depended on the virus sequence and was not necessarily reciprocal. Cell transfer studies showed that both CD4 and CD8 T cell populations from LCMV-immune mice were required to transfer protective immunity to naive hosts challenged with PV or VV. In the case of LCMV-immune versus naive mice challenged with VV, there was an enhanced early recruitment of memory phenotype interferon (IFN) gamma-secreting CD4(+) and CD8(+) cells into the peritoneal cavity and increased IFN-gamma levels in this initial site of virus replication. Studies with IFN-gamma receptor knockout mice confirmed a role for IFN-gamma in mediating the protective effect by LCMV-immune T cell populations when mice were challenged with VV but not PV. In some virus sequences memory cell populations, although clearing the challenge virus more rapidly, elicited enhanced IFN-gamma-dependent immunopathogenesis in the form of acute fatty necrosis. These results indicate that how a host responds to an infectious agent is a function of its history of previous infections and their influence on the memory T cell pool.</p>
dc.identifier.submissionpathgsbs_sp/1090
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentProgram in Immunology/Virology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages1705-15


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