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American Journal of Pathology, Vol 140, 1187-1194, Copyright © 1992 by American Society for Investigative Pathology
REGULAR ARTICLES |
SJ Pirruccello, H Nakamine, KW Beisel, KL Kleveland, M Okano, Y Taguchi, JR Davis, ML Mahloch and DT Purtilo
Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha 68198-6495.
In the course of evaluating the severe combined immunodeficiency mouse- human peripheral blood lymphocyte (SCID-PBL) model of lymphoproliferative disease, we noted hemagglutination occurring in peripheral blood smears of mice with serum human immunoglobulin levels greater than 1.0 mg/ml. The hemagglutinating process was mediated by human anti-mouse red cell antibodies of the IgM class, peaked at five to seven weeks post-transfer of 5 to 7 x 10(7) human PBL and was generally self limiting. However, death resulted in some mice when serum immunoglobulin levels were greater than 3.0 mg/ml. The most severely affected mice had hemagglutination induced congestion of liver, lungs and spleen. Several mice also had lesions consistent with graft-versus-host disease (GVHD) including focal hepatic necrosis and destruction of mouse splenic hematopoietic elements. The lesions associated with hemagglutination and GVHD in SCID-PBL mice are distinct from those associated with EBV-induced lymphoproliferation. Recognition of these pathologic processes are required for a thorough understanding of the SCID-PBL model.
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