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    Activated lymphocytes during acute Epstein-Barr virus infection

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    Authors
    Tomkinson, Blake E.
    Wagner, David K.
    Nelson, David L.
    Sullivan, John L.
    UMass Chan Affiliations
    Department of Pediatrics
    Graduate School of Biomedical Sciences
    Document Type
    Journal Article
    Publication Date
    1987-12-01
    Keywords
    Acute Disease; Adolescent; Adult; Antigens, Surface; Humans; Infectious Mononucleosis; Killer Cells, Natural; Lymphocyte Activation; Receptors, Immunologic; Receptors, Interleukin-2; T-Lymphocytes
    Life Sciences
    Medicine and Health Sciences
    
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    Link to Full Text
    http://www.jimmunol.org/content/139/11/3802
    Abstract
    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.
    Source

    J Immunol. 1987 Dec 1;139(11):3802-7.

    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/32702
    PubMed ID
    3119718
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