Figure 1.

Mechanisms by which acute stress may enhance skin immunity. Stage 1: The brain detects the presence of a stressor and informs/warns the body by releasing stress hormones. Stage 2: Stress hormones increase the affinity/expression of adhesion molecules on leukocytes and/or endothelial cells. Stage 3: This results in a selective margination of leukocytes within the vasculature of organs such as the skin. Stage 4a: Upon cessation of stress, and in the absence of immunologic challenge at the site of leukocyte margination, leukocytes demarginate and join the circulating leukocyte pool (14). Stage 4b: However, if the stressor is accompanied by an immune challenge at the site of leukocyte margination, leukocytes are recruited by chemokines and cytokines released at the site of antigen entry. Thus, a stressed organism, by virtue of having higher numbers of leukocytes available for recruitment at potential sites of challenge, may mount a more robust immune response than an unstressed organism. Stage 5: In addition to affecting leukocyte distribution, acute stress may increase immunopreparedness by increasing inflammatory mediator production/function and by enhancing antigen presentation, leukocyte recruitment, leukocyte activation, and effector cell function within the site of an immune reaction. Thus, stress hormones and changes in leukocyte distribution within the body may be systemic mediators, and cytokines and chemokines local mediators, of a stress-induced enhancement of immune function.