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Related Experiment Videos

Infectious tolerance

S Cobbold1, H Waldmann

  • 1Sir William Dunn School of Pathology, South Parks Road, Oxford, OX1 3RE, UK. stephen.cobbold@pathology.ox.ac.uk

Current Opinion in Immunology
|October 31, 1998
PubMed
Summary
This summary is machine-generated.

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Infectious tolerance, a thymus-independent process, can be induced through immune deviation. This involves a shift towards Th2 cytokines, potentially leading to T-regulatory cell generation for immune suppression.

Area of Science:

  • Immunology
  • Autoimmune Diseases
  • Transplantation Immunology

Background:

  • Infectious tolerance can be induced via multiple pathways, independent of the thymus or clonal deletion.
  • Mechanisms like linked, bystander, or epitope suppression allow tolerance to spread to associated antigens.
  • Understanding these mechanisms is crucial for managing autoimmune diseases and transplantation outcomes.

Purpose of the Study:

  • To review evidence on the mechanisms of infectious tolerance.
  • To propose a consistent hypothesis for tolerance induction in Th1-mediated diseases and transplantation.
  • To elucidate the role of cytokine profiles and T cell subsets in immune suppression.

Main Methods:

  • Literature review of existing evidence on infectious tolerance.

Related Experiment Videos

  • Analysis of mechanisms involving immune deviation and cytokine production.
  • Hypothesis generation based on current understanding of T cell subsets and regulatory mechanisms.

    • Main Results:

    • Tolerance induction involves a phase of immune deviation towards Th2 cytokines (e.g., IL-4, IL-10).
    • Interleukin-10 (IL-10) may induce anergy or nonresponsiveness.
    • Generation of Th3/T-regulatory-1 CD4+ T cells is implicated in downregulating antigen-presenting cells, possibly via TGF-beta.

    Conclusions:

    • Infectious tolerance induction involves a complex interplay of immune deviation and regulatory T cell generation.
    • The Th2 cytokine shift and subsequent IL-10 effects are key components.
    • Th3/T-regulatory-1 cells play a critical role in suppressing immune responses through mechanisms like TGF-beta signaling.