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.
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
Stephen M
SM
Anderton
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