It has become widely accepted in the past decade that Th1 and Th2 cells represent alternate states of function and gene expression of CD4¹ T cells (Mosmann and Coffman 1989; Abbas et al. 1996). A question central to understanding the relevance of these subsets is whether they are products of an irreversible differentiation process or whether Th1 and Th2 cytokine patterns can be interchanged in an ordered or a regulated manner. Many disease states can be attributed to the activity of one specific Th subset, such as Th1-mediated autoimmune diseases or Th2-mediated allergic diseases and this implies that the ability to alter or reverse Th differentiation is a potential strategy for the treatment of such diseases.