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Figure 1 | Critical Care

Figure 1

From: Bench-to-bedside review: β-Adrenergic modulation in sepsis

Figure 1

T-helper type 1 and T-helper type 2 balance and the adrenergic system. Naive CD4+, T-helper type 0 (Th0) cells are bipotential and are precursors of T-helper type 1 (Th1) cells and T-helper type 2 (Th2) cells. IL-12, produced by antigen-presenting cells, is the major inducer of Th1 differentiation. Th1 and Th2 responses are mutually inhibitory. IL-12 and IFNγ therefore inhibit Th2 cell activity, while IL-4 and IL-10 inhibit the Th1 response. The stimulation of β-adrenergic receptors potently inhibits the production of IL-12 by antigen-presenting cells, and thus inhibits the development of Th1 cells while promoting Th2 cells.

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