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The Role of Mig, the Monokine Induced by Interferon- , and IP-10, the Interferon--Inducible Protein-10, in Tissue Necrosis and Vascular Damage Associated With Epstein-Barr Virus-Positive Lymphoproliferative Disease
Julie Teruya-Feldstein,
Elaine S. Jaffe,
Parris R. Burd,
Hirokazu Kanegane,
Douglas W. Kingma,
Wyndham H. Wilson,
Dan L. Longo, and
Giovanna Tosato
From the Laboratory of Pathology, Hematopathology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD; the Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD; the Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD; and the National Institute on Aging, National Institutes of Health, Baltimore, MD.
The mechanisms of tissue necrosis and vascular damage characteristics of certain Epstein-Barr virus (EBV)-associated lymphoproliferative disorders are unknown. The CXC chemokines interferon- -inducible protein-10 (IP-10) and the monokine induced by interferon- (Mig) caused tissue necrosis and vascular damage in Burkitt's lymphoma tumors established in nude mice. We report higher levels of IP-10 and Mig gene expression in tissues with necrosis and vascular damage from EBV-positive lymphomatoid granulomatosis and nasal or nasal-type T/natural killer (NK)-cell lymphomas compared with tissues with lymphoid hyperplasia, which lacked tissue necrosis and vascular damage. By immunohistochemistry, Mig and IP-10 proteins localized with similar patterns in viable tissue surrounding dead tissue, mostly within endothelial cells, monocyte/macrophages, and lymphocytes. Circulating levels of IP-10 were abnormally elevated in patients with EBV-positive lymphomatoid granulomatosis and nasal or nasal-type T/NK-cell lymphomas. These experiments provide the first description of the presence of Mig in any human normal or diseased tissue and the first description of IP-10 in certain lymphoproliferative lesions. These data suggest that Mig and IP-10 play an important role in the pathogenesis of tissue necrosis and vascular damage associated with certain EBV-positive lymphoproliferative processes.
Blood, Vol. 90 No. 10 (November 15), 1997:
pp. 4099-4105
© 1997 by The American Society of Hematology.
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