SPRINGER SEMINARS IN IMMUNOPATHOLOGY
|
1999年
/
21卷
/
03期
基金:
英国惠康基金;
关键词:
D O I:
暂无
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Because Th1/Th2 balance is perturbed during immunological disease, the design of strategies aiming at its rectification has become a priority. The alteration of the balance in pregnancy so as to promote survival of the fetal allograft lends credibility to this aim. Attenuation of the activation signal delivered through the T cell receptor (TCR) represents a promising approach. It is supported by the high level of poly morphism in the MHC class IT promoter, which regulates the natural TCR signal and thus modulates Th1/Th2 differentiation. Further support comes from the Th2 shift that occurs in JNK knockout mice, and with kinase inhibitors and anti-CD4 monoclonal antibodies applied in vitro. The approach has implications for nasal tolerance and inhibition of IL-12 production. The further range of options for Th1/Th2 modulation, which are presented throughout this issue of the journal, are here summarised and evaluated.