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Abstract: Recent evidence indicates that glucocorticoids and catecholamines, the major stress hormones, inhibit the production of proinflammatory cytokines, such as interleukin (IL)‐12, tumor necrosis factor (TNF)‐α, and interferon (IFN)‐γ, whereas they stimulate the production of antiinflammatory cytokines, such as IL‐10, IL‐4, and transforming growth factor (TGF)‐β. Thus, systemically, an excessive immune response, through activation of the stress system, stimulates an important negative feedback mechanism, which protects the organism from an “overshoot” of proinflammatory cytokines and other products of activated macrophages with tissue‐damaging potential. Conversely, in certain local responses and under certain conditions, stress hormones actually may boost regional immune responses, through induction of TNF‐α, IL‐1, and IL‐8, and by inhibiting TGF‐β production. Therefore, conditions that are …