In contrast to the preferential expression of AR by mouse Th2 cells, we have now shown that synthesis of human AR is not restricted to a particular human T cell subset. AR can be produced by activated naive and memory CD4 and CD8 T cells, including Th1 and Th2 phenotypes. Our results suggest that AR is not a specific product of certain pre-committed effector subsets of human CD4 T cells, but instead is regulated mainly by additional signals present during T cell activation, particularly signals influencing the cAMP signaling pathway. The lack of precommitment suggests that, in contrast to the memory of effector functions carried by T cells committed to Th1, Th2, Th17 etc phenotypes, the amount of AR produced in a particular immune response is regulated by the local environment during that response, but is less influenced by previous immune priming. The discrepancy we have identified between mouse and human T cell regulation highlights the importance of performing cross-species comparisons of effector T cell phenotypes.