Multiple analysis of the pathogenic mechanism of an re-emerging infectious disease, neonatal TSS-like exanthematous disease and related diseases

1998年，我们阐明了一种由超抗原毒素引起的传染病的发病机制，并将其命名为新生儿TSS样红斑病(NTT)。在目前的项目中，我们研究了以下主题：1)NTT患者的T细胞反应：TSST-1反应性T细胞在急性期增加到对照水平的3倍，1-2个月后下降到对照水平的20%。处于扩增状态的TSST-1反应性CD4+T细胞处于失能状态。3)超抗原诱导的小鼠T细胞反应：在植入SEA渗透泵的小鼠体内，发现SEA反应性的CD4+T细胞表现出长时间的扩增和记忆型反应。

In 1998 we have clarified the pathogenic mechanism of an infectious disease caused by a superantigenic toxin, and designated this disease neonatal TSS-like exanthematous disease (NTED). Under the current project, we examined following subjects.1) T cell response in patients with NTED: TSST- 1-reactive T cells increased to 3-fold the control level in the acute phase and decreased to 20% of the control level 1-2 months later. TSST-1-reactive CD4+ T cells in expanded state are in an anergic state. The presence of IgG-type antibodies to TSST-1 prevented manifestation of clinical symptoms in MRSA neonatal carriers.2) Responsibility of T cell in neonates: We obtained data suggesting that susceptibility of T cells in neonates to anergy induction to TSST-1 is caused by an inability of tyrosine-kinase Lck to make functional association with tyrosine-phosphatase CD45. 3) Superantigen-induced T cell response in mice: Using mice implanted with an osmotic pump filled with SEA, it was found that SEA-reactive CD4+ T cells exhibited protracted expansion and a memory-type response. 4) Discovery of a new type of superantigenic toxin: We found a new type of superantigenic toxin, Streptococcus dysgalactiae-derived mitogen which activates Yβ1 + and Vβ23+ T cells in association with MHC class II molecules on antigenpresenting cells.