Attrition of virus-specific memory CD8+ T cells during reconstitution of lymphopenic environments
| dc.contributor.author | Peacock, Craig D. | |
| dc.contributor.author | Kim, Sung-Kwon | |
| dc.contributor.author | Welsh, Raymond M. | |
| dc.date | 2022-08-11T08:09:31.000 | |
| dc.date.accessioned | 2022-08-23T16:34:00Z | |
| dc.date.available | 2022-08-23T16:34:00Z | |
| dc.date.issued | 2003-07-09 | |
| dc.date.submitted | 2009-03-10 | |
| dc.identifier.citation | <p>J Immunol. 2003 Jul 15;171(2):655-63.</p> | |
| dc.identifier.issn | 0022-1767 (Print) | |
| dc.identifier.doi | 10.4049/jimmunol.171.2.655 | |
| dc.identifier.pmid | 12847230 | |
| dc.identifier.uri | http://hdl.handle.net/20.500.14038/38233 | |
| dc.description.abstract | Viruses can cause a severe lymphopenia early in infection and a subsequent, lasting loss of pre-existing CD8(+) memory T cells. We therefore questioned how well virus Ag-specific memory CD8(+) T cells could reconstitute mice rendered lymphopenic as a consequence of genetics, irradiation, or viral or poly(I:C)-induced cytokines. In each case, reconstitution of the CD8(+) compartment was associated with limited division of virus-specific memory T cells and a reduction in their proportion. This indicates that foreign Ag-experienced CD44(high)CD8(+) memory T cells may respond differently to homeostatic signals than other CD44(high)CD8(+) cells, and that events inducing lymphopenia may lead to a permanent reduction in T cell memory. | |
| dc.language.iso | en_US | |
| dc.relation | <p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=12847230&dopt=Abstract">Link to Article in PubMed</a></p> | |
| dc.relation.url | https://doi.org/10.4049/jimmunol.171.2.655 | |
| dc.subject | *Adoptive Transfer | |
| dc.subject | Animals | |
| dc.subject | Antigens, CD44 | |
| dc.subject | Apoptosis | |
| dc.subject | Arenaviridae Infections | |
| dc.subject | CD8-Positive T-Lymphocytes | |
| dc.subject | effects | |
| dc.subject | Epitopes, T-Lymphocyte | |
| dc.subject | Homeostasis | |
| dc.subject | *Immunologic Memory | |
| dc.subject | Lymphocyte Count | |
| dc.subject | Lymphocytic Choriomeningitis | |
| dc.subject | Lymphocytic choriomeningitis virus | |
| dc.subject | Lymphopenia | |
| dc.subject | Male | |
| dc.subject | Mice | |
| dc.subject | Mice, Inbred C57BL | |
| dc.subject | Mice, Knockout | |
| dc.subject | Mice, SCID | |
| dc.subject | Pichinde virus | |
| dc.subject | Radiation Chimera | |
| dc.subject | Spleen | |
| dc.subject | T-Lymphocyte Subsets | |
| dc.subject | Life Sciences | |
| dc.subject | Medicine and Health Sciences | |
| dc.title | Attrition of virus-specific memory CD8+ T cells during reconstitution of lymphopenic environments | |
| dc.type | Journal Article | |
| dc.source.journaltitle | Journal of immunology (Baltimore, Md. : 1950) | |
| dc.source.volume | 171 | |
| dc.source.issue | 2 | |
| dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/oapubs/1109 | |
| dc.identifier.contextkey | 770087 | |
| html.description.abstract | <p>Viruses can cause a severe lymphopenia early in infection and a subsequent, lasting loss of pre-existing CD8(+) memory T cells. We therefore questioned how well virus Ag-specific memory CD8(+) T cells could reconstitute mice rendered lymphopenic as a consequence of genetics, irradiation, or viral or poly(I:C)-induced cytokines. In each case, reconstitution of the CD8(+) compartment was associated with limited division of virus-specific memory T cells and a reduction in their proportion. This indicates that foreign Ag-experienced CD44(high)CD8(+) memory T cells may respond differently to homeostatic signals than other CD44(high)CD8(+) cells, and that events inducing lymphopenia may lead to a permanent reduction in T cell memory.</p> | |
| dc.identifier.submissionpath | oapubs/1109 | |
| dc.contributor.department | Department of Pathology | |
| dc.source.pages | 655-63 |
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