“…The present findings are consistent with previous data showing that myeloid lineage immune cells and their innate effector molecules, such as proinflammatory cytokines and type I interferons, are regulated by β-adrenergic signaling (7,(57)(58)(59)(60)(61)(62) and adverse socioenvironmental conditions (2,7,10,13,17,63). These results are also consistent with previous findings that nonsocial activators of β-adrenergic signaling, such as burn-induced sepsis, can enhance monocyte differentiation (28,29).…”