Exudation of eosinophil polymorphonuclear leukocytes (E-PMN) in response to tetanus toxoid (TT) was studied in DBA/2HaD mice with erythroleukemia induced by Friend virus (FV). The inhibition of exudation that developed was independent of increased levels of serum corticosteroids and occurred in surgically adrenalectomized mice. Thus it was independent of steroid-induced effects on E-PMN. The accumulation of neutrophil polymorphonuclear leukocytes (N-PMN) in TT-induced exudates was unaltered. Furthermore, N-PMN exudation in response to other inflammatory stimuli was similarly unimpaired in virus-infected mice, which confirmed the specificity of the inhibition for E-PMN. The virus entity in the FV complex responsible for the effect was not identified. Friend murine leukemia virus, the indigenous helper virus for the defective spleen focus-forming virus, alone, was incapable of inducing the inhibition. It is possible that the lack of participation of E-PMN in TT-induced immune inflammatory exudates in FV-infected mice reflects an unresponsiveness that contributes to the development and progression of leukemia in FV-infected mice.