Stress and the Immune System

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Physical and psychosocial stressors have been shown to compromise immune function (Ader et al., 1991; Kielcolt-Glaser and Glaser, 1995). The immune suppressive effects of stress may be more pronounced in individuals that already have limited immune competence, such as infants, individuals with a predisposition to autoimmune disease, and the elderly (Kielcolt-Glaser and Glaser, 1995). An individual's response to a stressor is manifested in physiological, hormonal, behavioral, and immunological changes. These stress-induced responses are initiated by the hypothalamus and translated into action by the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system. Products from these two systems (e.g., corticoid hormones and catecholamines) can directly modulate the activity of various immune effector cells (Ader et al., 1991).

Stress has a bidirectional effect on the immune system depending on whether it is acute or chronic. Acute stress enhances antigen-specific cell-mediated immunity (Dhabhar and McEwen, 1996), alters populations of T-cell subsets (Teshima et al., 1987) and modulates mononuclear cell trafficking (Hermann et al., 1995). Acute stressors augment the immune response and result in redistribution of immune cells from the bone marrow into the blood, lymph nodes, and skin (Dhabhar and McEwen, 1996). Redeployment of immune cells into these compartments will allow for heightened responsiveness in the event of a skin wound, a natural consequence of an encounter with a predator as the acute stressor. Likewise, T cell and natural killer cell function are altered by stressful events (Okimura et al., 1986). In contrast, chronic stressful life events are thought to suppress the ability of the immune system to respond to challenge and thus increase susceptibility to infectious diseases and cancers.

Although there is convincing evidence linking stress with the onset and progression of certain infectious diseases (e.g., influenza, herpes), relatively little is known about the role of stress in autoimmune diseases (e.g., multiple sclerosis, rheumatoid arthritis, lupus, insulin-dependent diabetes). However, a few studies indicate that stressful life events and poor social support play a role in the onset and exacerbation of autoimmune diseases such as rheumatoid arthritis (Rimon et al., 1977; Homo-Delarche et al., 1991). Furthermore, intervention studies indicate that cognitive-behavioral stress management decreases the symptomatology of autoimmune disease (Bradley et al., 1987; O'Leary et al., 1988; Radojevic et al., 1992).

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