T-cell signalling and autoimmunity: molecular mechanisms of disease.
The genetic manipulation of mice has led to insights into the molecular mechanisms of autoimmune disease. Recent studies have begun to identify ways in which signalling cascades can be disrupted that preclude the development of autoimmunity. This review outlines a new model for the induction of T-cell-mediated autoimmune diseases. I highlight recent data that illustrate the ways in which the altered survival of T cells and defects in the inhibitory signalling pathways of T cells can contribute to autoimmunity.
Ohashi
Pamela S
PS
Ontario Cancer Institute, University Health Network, Department of Medical Biophysics, University of Toronto, Canada. pohashi@uhnres.utoronto.ca
D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology; D015551:Autoimmunity; D051858:Forkhead Transcription Factors; D006801:Humans; D051379:Mice; D018448:Models, Immunological; D018716:Molecular Mimicry; D009687:Nuclear Proteins / Q000276:immunology; D019869:Phosphatidylinositol 3-Kinases / Q000276:immunology; D011518:Proto-Oncogene Proteins / Q000276:immunology; D050721:Proto-Oncogene Proteins c-cbl; D011948:Receptors, Antigen, T-Cell / Q000378:metabolism; D017634:Self Tolerance; D015398:Signal Transduction / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*; D014157:Transcription Factors / Q000276:immunology; D044767:Ubiquitin-Protein Ligases
D051858:Forkhead Transcription Factors; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D011948:Receptors, Antigen, T-Cell; D014157:Transcription Factors; D050721:Proto-Oncogene Proteins c-cbl; D044767:Ubiquitin-Protein Ligases; D019869:Phosphatidylinositol 3-Kinases; C067419:CBL protein, human; C493849:Cbl protein, mouse