Interleukin-18, interferon-γ, IP-10, and Mig expression in Epstein- Barr virus-induced infectious mononucleosis and posttransplant lymphoproliferative disease

Joyce Setsuda, Julie Teruya-Feldstein, Nancy L. Harris, Judith A. Ferry, Lynn Sorbara, Ghanshyam Gupta, Elaine S. Jaffe, Giovanna Tosato

Research output: Contribution to journalArticlepeer-review

57 Scopus citations

Abstract

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-γ (IFN-γ), 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-γ, 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-γ, 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.

Original languageEnglish
Pages (from-to)257-265
Number of pages9
JournalAmerican Journal of Pathology
Volume155
Issue number1
DOIs
StatePublished - Jul 1999
Externally publishedYes

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