ADMINISTRATION OF RABBIT ANTI-ASIALO GM1 ANTISERUM FACILITATES THE DEVELOPMENT OF HUMAN EPSTEIN-BARR VIRUS-INDUCED LYMPHOPROLIFERATIONS IN XENOGRAFTED C.B-17 SCID SCID MICE/

Mice with severe combined immune deficiency (C.B-17 scid/scid [SCID mi ce]) lack functional B and T lymphocytes and are permissive for the gr owth of human xenografts. However, the development of functional Nh ce lls is not affected by the scid mutation. Mouse Nh cells express the s urface glycolipid asialo GM1 and are implicated in the rejection of he terotransplanted cells. In the present study, we demonstrate that SCID mice treated with rabbit anti-asialo GM1 antiserum (cu-asialo GM1), f or in vivo depletion of endogenous Nh cell function, develop lethal Ep stein-Barr virus (EBV)-induced lymphoproliferative disorders (EBV-LPD) at lower doses of inoculated EBV-transformed lym-phoblastoid B cell l ines (EBV-LCL) than untreated animals. Furthermore, at any given dose of EBV-LCL inoculated, EBV-LPD developed earlier and induced lethality sooner in alpha-asialo GM1-treated animals. We also demonstrate that SCID mice treated with alpha-asialo GM1 have a reduction in the number of asialo GM1-expressing splenocytes. Moreover, splenic cell suspensi ons derived from alpha-asialo GM1-treated SCID mice show lower cytotox icity against the mouse MK-sensitive cell line YAC-1 and human EBV-LCL than splenocytes obtained from untreated SCID mice.