T cell control of staphylococcal enterotoxin B (SEB) lethal sensitivity inmice: CD4(+) CD45RB(bright)/CD4(+) CD45RB(dim) balance defines susceptibility to SEB toxicity

Radiation chimeras, generated by transplantation of SCID bone marrow into C 3H/HeJ mice, show lethal susceptibility to staphylococcal enterotoxin B (SE B), thus constituting a valid murine model for SEE shock. This SEE sensitiv ity 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 cell s. SCID bone marrow transplanted into irradiated nude mice does not generat e SEE-sensitive chimeras, as a consequence of the inability of the recipien t nude mice to develop mature T cells. Thymectomy of normal recipient mice prior to bone marrow transplantation does not affect the development of sus ceptibility to SEE, suggesting that post thymic, residual T cells of the ho st probably mediate this SEE sensitivity. In vivo depletion experiments sho w that CD4(+) T cells are required for the SEE-triggered shock, while CD8() cells suppress it. A further examination of the T helper subpopulations i n the SEE-sensitive mice reveals a prevalence of CD4(+)CD45RB(dim) cells ov er CD4(+)CD45RB(bright) cells. This T helper balance was statistically sign ificant when correlated with SEE-induced mortality. Our model provides a po ssible explanation for the SEE resistance of normal mice: they have a preva lence of CD4(+)CD45RB(dim) over CD4(+)CD45RB(bright) cells.