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A unique type of hypersensitivity-ETH was previously reported
to be distinct from the traditional four types of
hypersensitivity. When antigen was given intravenously into
antigen-primed mice, anaphylaxis was induced. The GAT or ConA
stimulated T-cell proliferation was also inhibited. The
hyporesponsiveness induced by anaphylaxis occurred only on
certain situations and it can not be reversed by exogeneous
IL-2, neither be explained by the involvement of apoptosis.
The drugs were used to block the anaphylaxis associated
hyporesponsiveness. Only cyproheptadine can partially reverse
the effect, suggesting that histamine or serotonin might
involve in the induction of hyporesponsiveness. We found SEB
also induced anaphylatic death on SEB/CFA-sensitized mice. T
cell proliferation to SEB or Con A was also inhibited after SEB-
induced anaphylaxis. The SEB-induced nonresponse is not
correlate to the downregulation of IL-2R. But it seems to
correlate with activation-induced cell death. Pretreating the
mice with cyproheptadine or dexamethasone can partially inhibit
the effect, suggesting that histamine or glucocorticoid
inhibitable mediator be involved in the induction of
hyporesponsiveness. The immunophenotype was determined by
three -color analysis,after SEB injection on naive or SEB/CFA
primed mice. We found that in naive mice ，SEB caused the
reduction of Vb8+CD45RB+ splenocytes at 12hr. These population
will expand at 24hr and depleted again at 72 hr. But Vb8+CD45
RB- splenocytes seemed to be resistant to the SEB stimulation.
There was a small size Vb8+CD4-CD8- subset can expand after SEB
stimulation. In the lymph nodes, Vb8+CD4+ was deleted at 24
hr. No expansion followed by deletion of Vb8+ cells was found.
The Vb8+CD4-CD8- cells would develop after SEB stimulation at
72hr.
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