Stress and Disease Processes

By Neil Schneiderman; Philip McCabe et al. | Go to book overview

2
Stress and Immunity

Jan A. Moynihan Nicholas Cohen University of Rochester School of Medicine and Dentistry

Research conducted at three levels of biological complexity has revealed bidirectional communication between the central nervous system (CNS) and the immune system. Studies at the level of molecular and cellular events have pointed out that macrophages and lymphocytes express surface receptors for many neuropeptides and hormones ( Bost, 1988), that macrophage-like glial cells of the CNS produce cytokines such as interleukin-I (IL-1) and IL-6 ( Beneviste, 1988), and that mitogen- or antigen-stimulated lymphocytes produce hormones including proopiomelanocortin-derived peptides, thyrotropin, prolactin, and growth hormone ( Blalock, 1988). Numerous other studies have revealed that the interactions of hormones and neurotransmitters with their specific receptors on immunocytes signal alterations in immunologically relevant events such as lymphocyte proliferation, activity of natural killer (NK) cells, antibody production, the expression of cytokine receptors, and cytokine synthesis and release ( Bernton, Bryant, & Holaday 1991; Goetzl, Turck, & Sreedharan, 1991; Heijnen, Kavelaars, & Ballieux, 1991; Kelley, 1991; Madden & Livnat, 1991; McCruden & Stimson, 1991; McGillis, Mitsuhashi, & Payan, 1991; Munck & Guyre, 1991; Ottaway, 1991). Experiments at the organ system level indicate that lymphoid tissues are richly innervated ( Felten & Felten, 1991) and that abrogation of this sympathetic innervation alters immunity ( Madden & Livnat, 1991). Thus, lines of communication between the nervous, endocrine, and immune systems are in place. Finally, experiments at the organismic level involving classical conditioning on the one hand, and "stress" on the other, point out that the immunomodulatory interactions between the CNS and the immune system are behaviorally driven and

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