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PubMed · 9794831

Infectious tolerance.

S Cobbold·H Waldmann
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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.

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AnimalsHumansImmune ToleranceInfectionsTh1 CellsTh2 CellsTransforming Growth Factor betaJournal ArticleReview

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S Cobbold, H Waldmann. 1998. Infectious tolerance.. https://doi.org/10.1016/s0952-7915(98)80217-3

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