Abstract

Directing both innate and adaptive immune responses against foreign pathogens with correct timing, location and specificity is a fundamental objective for the immune system. Full activation of CD4⁺ T cells requires the binding of peptide–MHC complexes coupled with accessory signals provided by the antigen-presenting cell. However, aberrant activation of the T-cell receptor alone in mature T cells can produce a long-lived state of functional unresponsiveness, known as anergy. Recent studies probing both immune signalling pathways and the ubiquitin–proteasome system have helped to refine and elaborate current models for the molecular mechanisms underlying T-cell anergy. Controlling anergy induction and maintenance will be a key component in the future to mitigate unwanted T-cell activation that leads to autoimmune disease.

Author affiliations

1. Stanford University School of Medicine, Department of Medicine, Division of Immunology and Rheumatology, CCSR Building, 269 Campus Drive, Room 2225, Stanford, California 94305-5166, USA.

Correspondence to: C. Garrison Fathman¹ Email: cfathman@stanford.edu

Published online 6 July 2007

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