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, IP-10, and Mig Expression in Epstein-Barr Virus-Induced Infectious Mononucleosis and Posttransplant Lymphoproliferative Disease
From the Laboratory of Pathology,*
Hematopathology
Section, National Cancer Institute, National Institutes of Health,
Bethesda, Maryland; the Department of
Pathology,
Massachusetts General Hospital,
Harvard University Medical School, Boston, Massachusetts; and the
Center for Biologics Evaluation and Research,
Food and Drug Administration, Bethesda, Maryland
T cell immunodeficiency plays an important role in the pathogenesis
of posttransplant lymphoproliferative disease (PTLD) by permitting the
unbridled expansion of Epstein-Barr virus (EBV)-infected B lymphocytes.
However, factors other than T cell function may contribute to
PTLD pathogenesis because PTLD infrequently develops even in the
context of severe T cell immunodeficiency, and athymic mice
that are T-cell-immunodeficient can reject EBV-immortalized cells. Here
we report that PTLD tissues express significantly lower levels of
IL-18, interferon-
(IFN-), Mig, and
RANTES compared to lymphoid tissues diagnosed with acute EBV-induced
infectious mononucleosis, as assessed by semiquantitative
RT-PCR analysis. Other cytokines and chemokines are expressed at
similar levels. Immunohistochemistry confirmed that PTLD tissues
contain less IL-18 and Mig protein than tissues with infectious
mononucleosis. IL-18, primarily a monocyte product,
promotes the secretion of IFN-, which stimulates Mig and
RANTES expression. Both IL-18 and Mig display antitumor activity in
mice involving inhibition of angiogenesis. These results document
greater expression of IL-18, IFN-, Mig, and
RANTES in lymphoid tissues with acute EBV-induced infectious
mononucleosis compared to tissues with PTLD and raise the possibility
that these mediators participate in critical host responses to EBV
infection.
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