The elucidation of the mechanism and pathogenesis of severe drug eruption.

肺炎支原体（Mycoplasma pneumoniae， MP）感染与重症药疹型史蒂文斯-约翰逊综合征（Stevens-Johnson syndrome， SJS）的发病有关。然而，其因果关系尚不清楚。我们之前发现调节性T（Treg）细胞的功能活性在SJS急性期受损。因此，我们研究Treg细胞是否与SJS的发生有关。在MP、水痘带状疱疹病毒和细小病毒B19感染的急性期，Tregs的功能活性严重受损。特别是，在MP感染中，Treg功能受损与CCR6+Treg的减少有关，而与其他病毒感染无关。然而，在病毒感染后，受损的Treg功能得以恢复，而在MP感染后1年，Treg功能仍未恢复。我们的研究结果表明，MP感染可以通过长期废除treg介导的抑制来增加随后发展为严重过敏性疾病的风险。

Mycoplasma pneumoniae(MP) infection is related in the pathogenesis of Stevens-Johnson syndrome(SJS) which is severe drug eruption. However, its causal relationship is unclear. We previously found that the functional activity of regulatory T(Treg) cells was impaired in the acute stage of SJS. We therefore investigated whether Treg cells were related to development of SJS. The functional activity of Tregs was profoundly impaired during the acute phase of infection with MP, varicella-zoster virus, and parvovirus B19.In particular, the impaired Treg function was associated with a decrease in the CCR6+Tregs in infection with MP but not with other viral infections. Upon resolution, however, the impaired Treg function had been restored in viral infections, while it remained abrogated even 1year after infection with MP. Our findings suggest that MP infections could serve to enhance the risk of subsequently developing severe allergic diseases by chronically abrogating Treg-mediated suppression.