title: Natural and induced regulation of Th1/Th2 balance.
abstract: 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 polymorphism in the MHC class II 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.
authors.affiliation: Department of Immunology, University College London, Windeyer Institute of Medical Sciences, UK.
authors.forename: N A
authors.initials: NA
authors.lastname: Mitchison
authors.forename: D
authors.initials: D
authors.lastname: Schuhbauer
authors.forename: B
authors.initials: B
authors.lastname: Müller
mesh_terms: D000818:Animals; D002450:Cell Communication / Q000276:immunology; D002454:Cell Differentiation; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D051379:Mice; D018345:Mice, Knockout; D011247:Pregnancy; D011948:Receptors, Antigen, T-Cell / Q000235:genetics / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D011948:Receptors, Antigen, T-Cell