Avoiding autoimmune disease--T cells know their limits.
The molecular mimicry theory has become a dominant paradigm to explain the triggering of autoaggressive T lymphocytes. The basis of the theory is that an immune response is triggered by non-self during infection and subsequent cross-reactive T-cell recognition of a similar self antigen provokes an inflammatory lesion in the target organ. It is clear that we all harbour autoreactive T cells and that T-cell receptor (TCR) cross-reactivity is extensive. Here, I argue that the immune system has evolved mechanisms to limit the risk of an autoaggressive response. Importantly, the strength of TCR stimulation provided by self and non-self antigens will usually differ. Evidence points to a model in which the three pillars of immune tolerance (deletion, anergy-adaptation and regulation) act to limit autoimmune disease from molecular mimicry.
Anderton
Stephen M
SM
University of Edinburgh, Institute of Immunology and Infection Research, School of Biological Sciences, Kings Buildings, West Mains Road, Edinburgh EH9 3JT, UK. steve.anderton@ed.ac.uk
D000220:Adaptation, Biological; D000818:Animals; D000941:Antigens / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology* / Q000473:pathology; D006801:Humans; D018448:Models, Immunological; D012307:Risk Factors; D013601:T-Lymphocytes / Q000276:immunology*
D000941:Antigens