title: Infectious tolerance.
abstract: Infectious tolerance can be induced in many ways, does not require a thymus or clonal deletion and can spread to third-party antigens linked on the same antigen-presenting cell-the process being variously described as linked-, bystanderor epitope-suppression. We here review the evidence concerning the mechanisms involved and attempt to make a consistent hypothesis, that during tolerance induction in the Th1-mediated autoimmune diseases and transplantation systems there would seem to be a phase of immune deviation towards Th2 cytokines, like IL-4 and IL-10; however, this may lead to an IL-10-induced form of anergy or nonresponsiveness and generation of the recently characterized Th3/T-regulatory-1 CD4+ T cell subset which is thought to downregulate the antigen-presenting cell, possibly via transforming growth factor beta.
authors.affiliation: Sir William Dunn School of Pathology, South Parks Road, Oxford, OX1 3RE, UK. stephen.cobbold@pathology.ox.ac.uk
authors.forename: S
authors.initials: S
authors.lastname: Cobbold
authors.forename: H
authors.initials: H
authors.lastname: Waldmann
mesh_terms: D000818:Animals; D006801:Humans; D007108:Immune Tolerance; D007239:Infections / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000502:physiology
chemical_list: D016212:Transforming Growth Factor beta