T-cell responses to dengue virus in humans
| dc.contributor.author | Kurane, Ichiro | |
| dc.contributor.author | Matsutani, Takaji | |
| dc.contributor.author | Suzuki, Ryuji | |
| dc.contributor.author | Takasaki, Tomohiko | |
| dc.contributor.author | Kalayanarooj, Siripen | |
| dc.contributor.author | Green, Sharone | |
| dc.contributor.author | Rothman, Alan L. | |
| dc.contributor.author | Ennis, Francis A. | |
| dc.date | 2022-08-11T08:11:05.000 | |
| dc.date.accessioned | 2022-08-23T17:32:35Z | |
| dc.date.available | 2022-08-23T17:32:35Z | |
| dc.date.issued | 2011-12-01 | |
| dc.date.submitted | 2012-06-22 | |
| dc.identifier.citation | Trop Med Health. 2011 Dec;39(4 Suppl):45-51. Epub 2011 Dec 1. <a href="http://dx.doi.org/10.2149/tmh.2011-S09">Link to article on publisher's site</a> | |
| dc.identifier.issn | 1348-8945 (Linking) | |
| dc.identifier.doi | 10.2149/tmh.2011-S09 | |
| dc.identifier.pmid | 22500136 | |
| dc.identifier.uri | http://hdl.handle.net/20.500.14038/50983 | |
| dc.description.abstract | Dengue virus (DENV) is a leading cause of morbidity and mortality in most tropical and subtropical areas of the world. Dengue virus infection induces specific CD4+CD8- and CD8+CD4- T cells in humans. In primary infection, T-cell responses to DENV are serotype cross-reactive, but the highest response is to the serotype that caused the infection. The epitopes recognized by DENV-specific T cells are located in most of the structural and non-structural proteins, but NS3 is the protein that is most dominantly recognized. In patients with dengue hemorrhagic fever (DHF) caused by secondary DENV infection, T cells are highly activated in vivo. These highly activated T cells are DENV-specific and oligoclonal. Multiple kinds of lymphokines are produced by the activated T cells, and it has been hypothesized that these lymphokines are responsible for induction of plasma leakage, one of the most characteristic features of DHF. Thus, T-cells play important roles in the pathogenesis of DHF and in the recovery from DENV infection. | |
| dc.language.iso | en_US | |
| dc.relation | <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=22500136&dopt=Abstract">Link to Article in PubMed</a> | |
| dc.subject | Life Sciences | |
| dc.subject | Medicine and Health Sciences | |
| dc.subject | Women's Studies | |
| dc.title | T-cell responses to dengue virus in humans | |
| dc.type | Journal Article | |
| dc.source.journaltitle | Tropical medicine and health | |
| dc.source.volume | 39 | |
| dc.source.issue | 4 Suppl | |
| dc.identifier.legacyfulltext | https://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1515&context=wfc_pp&unstamped=1 | |
| dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/wfc_pp/516 | |
| dc.identifier.contextkey | 3017573 | |
| refterms.dateFOA | 2022-08-23T17:32:35Z | |
| html.description.abstract | <p>Dengue virus (DENV) is a leading cause of morbidity and mortality in most tropical and subtropical areas of the world. Dengue virus infection induces specific CD4+CD8- and CD8+CD4- T cells in humans. In primary infection, T-cell responses to DENV are serotype cross-reactive, but the highest response is to the serotype that caused the infection. The epitopes recognized by DENV-specific T cells are located in most of the structural and non-structural proteins, but NS3 is the protein that is most dominantly recognized. In patients with dengue hemorrhagic fever (DHF) caused by secondary DENV infection, T cells are highly activated in vivo. These highly activated T cells are DENV-specific and oligoclonal. Multiple kinds of lymphokines are produced by the activated T cells, and it has been hypothesized that these lymphokines are responsible for induction of plasma leakage, one of the most characteristic features of DHF. Thus, T-cells play important roles in the pathogenesis of DHF and in the recovery from DENV infection.</p> | |
| dc.identifier.submissionpath | wfc_pp/516 | |
| dc.contributor.department | Center for Infectious Disease and Vaccine Research | |
| dc.contributor.department | Department of Medicine, Division of Infectious Diseases and Immunology | |
| dc.source.pages | 45-51 |
