Requirement of I-E molecule for thymocyte apoptosis induced by Staphylococcal enterotoxin B in vivo

In vivo administration of bacterial superantigen staphylococcal enterotoxin B (SEB) to BALB/c mice led to thymus atrophy resulting from thymocyte apoptosis. In this study, we demonstrated that SEB induced a substantial reduction in thymocyte numbers in BALB/c, B10.D2 (H-2(d) haplotype), B10.BR, C3H/HeJ, C3H/HeN (H2(k)), and (BALB/c x B6)F1 (H-2(dxb)), but caused little or no effect in I-E^- strains such as B6, B10, A.BY (H- 2^b), and A.SW (H-2^b) mice. Elimination of CD4⁺CD8⁺ cells predominantly accounted for the thymocyte loss, although the numbers of other subpopulations may also be reduced. Thymocyte apoptosis was shown by an increase in the level of DNA fragmentation in BALB/c but not in B6 mice after SEB administration. Treatment with anti-I-E(d) monoclonal antibody to BALB/c mice blocked SEB-induced thymocyte apoptosis when anti-I-A(d) exerted less effect. In contrast to SEB, staphylococcal enterotoxin A led to comparable levels of thymus atrophy in BALB/c and B6 mice. Studies on the surface marker expression indicated that CD25 expression was upregulated on BALB/c mouse thymocytes but with only a moderate increase in B6 mice. The CD4⁺CD8⁺ cells were the major (>90%) population that expressed elevated levels of CD25 in BALB/c mice. An increase in the expression of TCRαβ, CD3, and CD69 surface markers was also observed on thymocytes from BALB/c mice, but not from I-E^- strains. The differential response of I-E⁺ and I-E^- mice to SEB maybe exploited as a model for the study of apoptosis in the thymus.