T Cell Control of Staphylococcal Enterotoxin B (seb) Lethal Sensitivity in Mice: Cd4(+) Cd45rb(Bright)/Cd4(+) Cd45rb(Dim) Balance Defines Susceptibility to Seb Toxicity

Radiation chimeras, generated by transplantation of SCID bone marrow into C3H/HeJ mice, show lethal susceptibility to staphylococcal enterotoxin B (SEB), thus constituting a valid murine model for SEB shock. This SEB sensitivity is due to the ability of the irradiated host to restore residual T cell populations, since the SCID donor bone marrow is unable to generate T cells. SCID bone marrow transplanted into irradiated nude mice does not generate SEB‐sensitive chimeras, as a consequence of the inability of the recipient nude mice to develop mature T cells. Thymectomy of normal recipient mice prior to bone marrow transplantation does not affect the development of susceptibility to SEB, suggesting that post‐thymic, residual T cells of the host probably mediate this SEB sensitivity. In vivo depletion experiments show that CD4+ T cells are required for the SEB‐triggered shock, while CD8+ cells suppress it. A further examination of the T helper subpopulations in the SEB‐sensitive mice reveals a prevalence of CD4+ CD45RBdim cells over CD4+ CD45RBbright cells. This T helper balance was statistically significant when correlated with SEB‐induced mortality. Our model provides a possible explanation for the SEB resistance of normal mice: they have a prevalence of CD4+ CD45RBdim over CD4+ CD45RBbright cells.