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dc.contributor.authorTomkinson, Blake E.
dc.contributor.authorWagner, David K.
dc.contributor.authorNelson, David L.
dc.contributor.authorSullivan, John L.
dc.date2022-08-11T08:08:49.000
dc.date.accessioned2022-08-23T16:09:28Z
dc.date.available2022-08-23T16:09:28Z
dc.date.issued1987-12-01
dc.date.submitted2009-01-13
dc.identifier.citation<p>J Immunol. 1987 Dec 1;139(11):3802-7.</p>
dc.identifier.issn0022-1767 (Print)
dc.identifier.pmid3119718
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32702
dc.description.abstractActivated lymphocytes, as identified by HLA-DR expression, associated with acute Epstein-Barr virus (EBV)-induced infectious mononucleosis (IM) were shown to be a heterogeneous population containing significantly elevated cytotoxic/suppressor (CD8) T cells, natural killer (CD16) cells and helper (CD4) T cells. CD8 T cells were the primary activated population representing 24.5% of the total lymphocyte population. The activated CD4 T cells and natural killer cells accounted for 6.7% and 3.5% of the total lymphocyte population, respectively. Analysis of serum soluble interleukin 2 receptors (IL-2R) demonstrated significantly (p less than 0.001) elevated levels in the serum of acute IM patients compared with normal controls. Elevated levels of serum IL-2R were correlated (r = 0.67) with increased percentages of Leu 2a+/HLA-DR+T cells (i.e., activated CD8 T cells). Patients with X-linked lymphoproliferative syndrome and virus-associated hemophagocytic syndrome, two syndromes associated with severe acute EBV infections, demonstrated the most dramatic increase in serum IL-2R levels. These data demonstrate that EBV is associated with intense immune stimulation and that during acute IM activated lymphocytes, other than the CD8 T cells, may contribute to the immune response to EBV.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=3119718&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttp://www.jimmunol.org/content/139/11/3802
dc.subjectAcute Disease; Adolescent; Adult; Antigens, Surface; Humans; Infectious Mononucleosis; Killer Cells, Natural; Lymphocyte Activation; Receptors, Immunologic; Receptors, Interleukin-2; T-Lymphocytes
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleActivated lymphocytes during acute Epstein-Barr virus infection
dc.typeJournal Article
dc.source.journaltitleJournal of immunology (Baltimore, Md. : 1950)
dc.source.volume139
dc.source.issue11
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1259
dc.identifier.contextkey693171
html.description.abstract<p>Activated lymphocytes, as identified by HLA-DR expression, associated with acute Epstein-Barr virus (EBV)-induced infectious mononucleosis (IM) were shown to be a heterogeneous population containing significantly elevated cytotoxic/suppressor (CD8) T cells, natural killer (CD16) cells and helper (CD4) T cells. CD8 T cells were the primary activated population representing 24.5% of the total lymphocyte population. The activated CD4 T cells and natural killer cells accounted for 6.7% and 3.5% of the total lymphocyte population, respectively. Analysis of serum soluble interleukin 2 receptors (IL-2R) demonstrated significantly (p less than 0.001) elevated levels in the serum of acute IM patients compared with normal controls. Elevated levels of serum IL-2R were correlated (r = 0.67) with increased percentages of Leu 2a+/HLA-DR+T cells (i.e., activated CD8 T cells). Patients with X-linked lymphoproliferative syndrome and virus-associated hemophagocytic syndrome, two syndromes associated with severe acute EBV infections, demonstrated the most dramatic increase in serum IL-2R levels. These data demonstrate that EBV is associated with intense immune stimulation and that during acute IM activated lymphocytes, other than the CD8 T cells, may contribute to the immune response to EBV.</p>
dc.identifier.submissionpathgsbs_sp/1259
dc.contributor.departmentDepartment of Pediatrics
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages3802-7


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