Immune Restitution in Stress-Induced Immunosuppression

Author(s): Liang, W. -X., Stampfli, K.

Abstract: Following an introductory note on the stress concept proposed by Hans Selye in 1936, we draw the attention to the studies of Glaser and Kiecolt-Glaser, who have shown that psychic stress reactions increase the titers of humoral antibodies directed against opportunistic viruses such as EBV, CMV, and HSV-1 and at the same time weaken the cellular immune reactivity, as assessed in cytotoxic T cell reacticions against these viruses. These findings fit well into the observation of functionally antagonistic cytokine profiles in cell groups of the CD4+ helper cells as described Mosmann and Coffman. The Th-1 cells release mainly IL-2, II-12, and IFN-µ and thereby stimulate the cellular immune reactions. Conversely, the Th-2 cells produce predominantly IL-4, IL-6, and IL-10 thereby stimulating humoral immune reactions Recently it has been shown that the lymphokine profiles in Th-2 are linked to changes of the humoral balance between cortisol and dehydroepiandrosterone (DHEA). These studies show that there exist states of equilibrium between T- and B-cell-mediated immune reactions, which may selectively be altered in disfavor of T-cellular irnmunity by a stress-induced enhancement of cortisol release. An elevated level of cortisol also propagates the apoptotic elimination of immature thymocytes and reduces thereby the peripheralization of T lymphocytes. In an attempt to restitute stress-induced immunosuppression, a dampening of the cortisol release via a normalization of the production of corticotropin-releasing hormone (CRH) in the hypothalamus should, therefore, be of primary importance. Among the measures to attain this goal, the nutritive correction of an excessive macrophage stimulation, due to deficiency of antioxidants and to iron overload, deserves particular attention.

Keyword(s): Stress

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