FOXP3 and autoimmune disease: The subsequent identification of humans and mice deficient in CD4+CD25hi cells (as a result of mutations in the FOXP3 and Foxp3 genes respectively – see below), which develop severe autoimmune diseases (Sakaguchi et al., 1995, 1996; Chatila et al., 2000; Wildin et al., 2001) strongly suggests that these cells have a critical and non-redundant regulatory role in the maintenance of self-tolerance.