Figure 8: Sympathetic regulation of Th1 and Th2 cell balance. A, B) CD4+Th0 and Th1 cells express β2-ARs, but CD4+Th2 cells do not. APCs also express β2-ARs. These receptors provide a direct mechanism by which the SNS regulates Th cell differentiation and Th1 effector cell function. NE released from sympathetic nerves binds with β2-ARs expressed on the cell surface of Th0 and APCs mediate SNS regulation of Th1 and Th2 cell differentiation. Under normal conditions, the SNS drives the differentiation of Th2 cells by inhibiting the production of interferon-γ and IL-2 by Th0 cells, and also by reducing IL-12 and increasing IL-10 production by APCs. Ligand-receptor binding on differentiated Th1 cells modulates effector functions, most often reported to be suppressive. In contrast, Th2 cells lack β2-ARs, and therefore, the effects of the SNS on Th2 cells are indirect. (Green arrows, excitatory; red arrows, inhibitory).