Induction of monocyte procoagulant activity by murine hepatitis virus type 3 parallels disease susceptibility in mice

We have extended these observations by demonstrating that lymphocyte collaboration is necessary for the induction of monocyte PCA. When highly purified monocytes from C3H/St or BALB/c strains of mice are directly stimulated by the virus, no induction of PCA follows. These results parallel the PCA response to other stimuli (14) (15) (16) . In studies involving human PBM (41, 42) , we have observed that both helper and suppressor lymphocytes exist that appear central to the induction and regulation of the PCA response to LPS. Indeed, the induction of monocyte PCA by helper T cells can be markedly attenuated by Ty cells. This finding may be significant in explaining the response to MHV-3. It is possible that the failure of response by PBM from A/J mice could reflect an excess of suppressor cells rather than a lack of lymphocyte recognition and generation of triggered T helper cells. Furthermore, the different responses observed in C3H/St and BALB/c mice could reflect similar disproportions in the suppressor and helper cell participants. Another possible explanation of the differences in PCA induction by MHV-3 could reflect differences in the capacity of monocytes to receive signals from MHV-3-triggered lymphocytes or otherwise accept lymphocyte collaboration for this specific stimulus. The lack of a monocyte subpopulation (which is inducible) by MHV-3 within A/J mice might explain the failure of induction of PCA in this strain. Application of the cytologic PCA assay previously described (16) , in which we can visualize individual cells and the presence or absence of PCA, promises to provide additional information.