To confirm the protein results, influenza-specific CD69+ IFNc+ cells were sorted from two subjects (results from one subject are shown in Figure 5E) , and RT-PCR demonstrated that AR mRNA levels were strongly elevated in the IFNc+ influenza-specific cells AR is produced by T cell subsets expressing different chemokine receptors and surface markers. Chemokine receptors expressed selectively by T cell subsets lead to different homing and chemotactic properties. Expression patterns of chemokine receptors are partly but not entirely related to cytokine commitment patterns [36] [37] [38] [39] . Additional surface markers, including CD27 and the homing receptor CD62L are also expressed heterogeneously on human CD4 T cells. We therefore examined AR expression within subsets of memory CD4 T cells defined by the expression of these proteins. AR was produced at approximately similar frequencies by CD4 T cells positive or negative for the chemokine receptors CCR4, CCR7, CXCR3 and CXCR5, as well as CD62L and CD27 ( Figure 6 ). However, expression of the activation-induced protein CD69 was strongly correlated with AR expression, as seen in previous figures. Taken together with the data described above, AR expression appears to be a general ability of most or all subtypes of human T cells after TCR activation.