| pubmed-article:15463673 | pubmed:abstractText | Burnet and Fenner originally defined 'tolerance' as 'unresponsiveness against self'. It is now generally accepted that the phenomenon of tolerance is required to protect on individual from potentially autoreactive cells. Recent experiments have independently shown that parasite infection or interleukin 2 (IL-2) can reverse an established T-cell tolerance in vivo. Breaking T-cell tolerance restores the capacity of T cells to be stimulated by their specific antigen and, in the case of a self-antigen, may be followed by autoimmune disease. In this review, Martin Röcken and Ethan Shevach briefly describe the potential pathways for generating T-cell tolerance in vivo, and focus on recently described mechanisms by which parasitic infections may circumvent or abrogate the tolerant state. | lld:pubmed |
