Early-phase endotoxin tolerance was inducible in mice which were T cell deficient (nude), B cell deficient (xid), or asplenic, which suggests that these lymphoid cell subsets and the spleen do not contribute significantly to the induction of acquired lipopolysaccharide hyporesponsiveness. C3H/HeJ mice did not exhibit the hematopoietic changes observed in mice made endotoxin tolerant, which suggests that multiple mechanisms may underlie lipopolysaccharide hyporesponsiveness.