Type 1 diabetes, rheumatoid arthritis, and Crohn disease seem clinically diverse, but they arise from acommon problem: poor discrimination between self and nonself. The search for specific markers identifying the cells underlying tolerance, and the genetic basis of their development and function promises much-needed new treatments for autoimmune diseases, which affect about one in twenty of the world's population.1 A transcription factor called Foxp3 appears to be a prime player molecular basis of tolerance. This issue's Hot Papers documented how the molecular fox hunters found the first traces of their prey.123
Most autoreactive T cells – lymphocytes that target antigens expressed by healthy tissue – are destroyed as they mature in the thymus through a process of negative selection. Some autoreactive T cells escape negative selection, however, and enter the systemic circulation. The Hot Papers focus on a subgroup of T lymphocytes that express the glycoproteins CD4 and CD25. These ...
