Fig. 7.
Effective host barrier response against donor progenitors in the simultaneous absence of perforin-, FasL-, and TNFR1- or R2-dependent cytotoxic pathways.
(A) Cytotoxic double (perforin and FasL)–deficient B6-cdd recipients were either naive or primed with H-2bTNFR1−/− donor cells. Three weeks after priming, recipients received increasing doses of bone marrow (2 and 7 × 106 BMT-TCD) from the same splenectomized H-2b TNFR1−/− donors. The resistance in this triple knock-out model was examined by standard CFU-IL3 assay. (B-C) B6-cdd recipients were either naive or primed with H-2b TNFR2−/− donor cells. Three weeks after priming, recipients received 2.0 or 7.0 × 106 BMT-TCD from the same splectomized H-2b TNFR2−/−donors. Resistance was examined by CFU-IL3 (B) or CFU–GM-CSF assay (C).