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American Journal of Pathology, Vol 142, 139-147, Copyright © 1993 by American Society for Investigative Pathology

REGULAR ARTICLES

Characterization of clonality of Epstein-Barr virus-induced human B lymphoproliferative disease in mice with severe combined immunodeficiency

H Nakamine, AS Masih, M Okano, Y Taguchi, SJ Pirruccello, JR Davis, ML Mahloch, KW Beisel, K Kleveland and WG Sanger
Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha 68198-3135.

To improve the diagnostic accuracy and understanding of the pathogenesis of lymphoproliferative diseases (LPDs) occurring in immunosuppressed transplant recipients (post-transplantation LPD), clonality of Epstein-Barr virus-induced human LPDs in mice with severe combined immunodeficiency was examined by analyzing: 1) human immunoglobulin genes and their products, 2) the clonality of Epstein- Barr virus DNA, and 3) genetic alteration of c-myc or bcl-2 genes. A spectrum of clonality was found in the LPDs comparable with that reported for post-transplantation LPDs, although rearrangements of c- myc or bcl-2 genes were not detected. It is confirmed that this system is useful in terms of clonality for understanding the early phases in the pathogenesis of post-transplantation LPD or LPD in immune deficient patients.


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Copyright © 1993 by the American Society for Investigative Pathology.