Interleukin-18, interferon-gamma, IP-10, and Mig expression in Epstein-Barr virus-induced infectious mononucleosis and posttransplant lymphoproliferative disease
J. Setsuda et al., Interleukin-18, interferon-gamma, IP-10, and Mig expression in Epstein-Barr virus-induced infectious mononucleosis and posttransplant lymphoproliferative disease, AM J PATH, 155(1), 1999, pp. 257-265
Citations number
49
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
T cell immunodeficiency plays an important role in the pathogenesis of post
transplant lymphoproliferative disease (PTLD) by permitting the unbridled e
xpansion of Epstein-Barr virus (EBV)-infected B lymphocytes. However, facto
rs other than T cell function may contribute to PTLD pathogenesis because P
TLD infrequently develops even in the context of severe T cell immunodefici
ency, and athymic mice that are T-cell-immunodeficient can reject EBV-immor
talized cells. Here we report that PTLD tissues express significantly lower
levels of IL-18, interferon-gamma (IFN-gamma), Mig, and RANTES compared to
lymphoid tissues diagnosed with acute EBV-induced infectious mononucleosis
, as assessed by semiquantitative RT-PCR analysis. Other cytokines and chem
okines are expressed at similar levels. Immunohistochemistry confirmed that
PTLD tissues contain less IL-18 and Mig protein than tissues with infectio
us mononucleosis. IL-18, primarily a monocyte product, promotes the secreti
on of IFN-gamma, which stimulates Mig and RANTES expression. Both IL-18 and
Mig display antitumor activity in mice involving inhibition of angiogenesi
s, These results document greater expression of IL-18, IFN-gamma, Mig, and
RANTES in lymphoid tissues with acute EBV-induced infectious mononucleosis
compared to tissues with PTLD and raise the possibility that these mediator
s participate in critical host responses to EBV infection.