Molecular mechanisms of CD4+ T-cell anergy.
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.
Fathman
C Garrison
CG
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. cfathman@stanford.edu
Lineberry
Neil B
NB
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D017635:Clonal Anergy / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation / Q000276:immunology; D020543:Proteome / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology; D044767:Ubiquitin-Protein Ligases / Q000276:immunology
D020543:Proteome; D044767:Ubiquitin-Protein Ligases