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 apop tosis. In this study, we demonstrated that SEE induced a substantial reduct ion in thymocyte numbers in BALB/c, B10.D2 (H-2(d) haplotype), B10.BR, C3H/ HeJ, C3H/HeN (H-2(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 ASW (H-2(s)) mice. Elimination of CD4(+)CD8(+) cells predominantly accounted for the th ymocyte loss, although the numbers of other subpopulations may also be redu ced. Thymocyte apoptosis was shown by an increase in the level of DNA fragm entation in BALB/c but not in B6 mice after SEE administration. Treatment w ith anti-I-E-d monoclonal antibody to BALB/c mice blocked SEB-induced thymo cyte apoptosis when anti-I-Ad exerted less effect, In contrast to SEE,; sta phylococcal enterotoxin A led to comparable levels of thymus atrophy in BAL B/c and B6 mice. Studies on the surface marker expression indicated that CD 25 expression was upregulated on BALB/c mouse thymocytes but with only a mo derate increase in B6 mice. The CD4(+)CD8(+) cells were the major (>90%) po pulation that expressed elevated levels of CD25 in BALB/c mice. An increase in the expression of TCR alpha beta, CD3, and CD69 surface markers was als o observed on thymocytes from BALB/c mice, but not fi om I-E- strains. The differential response of I-E+ and I-E mice to SEE may be exploited as a mod el for the study of apoptosis in the thymus. (C) 1999 Academic Press.