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Staphylococcal enterotoxin B (SEB) is a member of enterotoxins
secreted by Staphylococcus aureus . SEB stimulates T cells
which bear specific Vb segment of T cell receptor (TCR).
Recent studies indicate that in addition to stimulation of
peripheral T cells, SEB induces programmed cell death
(apoptosis) in immature thymocytes. Furthermore, a repeated
stimulation of mature T cells results in a state of anergy.
Previous studies in our laboratory demonstrated that
administration of SEB resulted in the induction of apoptosis
especially in immature CD4+CD8+ thymocytes.
Glucocorticosteroid has been shown to induce apop- tosis in
immature thymocyte both in vivo and in vitro. We first
investigate whether thymic hormones might protect thymocytes
from SEB-induced apoptosis. Results show that after
administration of partially purified thymic hormone to SEB-
primed mice, the thymus weight, thymocyte numbers, and immature
CD4+CD8+, TCRablow, and Thy1.2high thymocyte subpopulations are
partially elevated as compared with the mice treated with SEB
alone. Further studies indicate that thymosin b4, but not
ProTa, partially reverse SEB- induced thymus atrophy. It has
been known that castration causes enlargement of thymus, our
data indicate that thymus shrinkage induced by SEB could not be
reversed by castration. On the other hand, SEB-induced thymus
atrophy is partially reversed by adrenalectomy. In studies of
SEB-induced hyporesponsiveness of peripheral T lymphocytes, the
results show that in vivo SEB- primed splenocytes exhibit a
reduced level of cell proliferation in response to SEB and anti-
CD3 mAb, but not to SEA. The SEB-, SEA-, or Con A-stimulated
IL-2 production appeared to reduced in splenocytes previously
primed with SEB. By third and fourth days following SEB
administration, 200 U/ml of IL-2 reverse the cell proliferation
to the control level, whereas 50 and 100 U/ml of IL-2 fail to
do the same.
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