This research was supported by the MacArthur Foundation and the DeWitt Wallace Foundation.
Stress-Induced Enhancement of Cell-Mediated Immunitya
Article first published online: 7 FEB 2006
Annals of the New York Academy of Sciences
Volume 840, NEUROIMMUNOMODULATION: MOLECULAR ASPECTS, INTEGRATIVE SYSTEMS, AND CLINICAL ADVANCES pages 359–372, May 1998
How to Cite
DHABHAR, F. S. (1998), Stress-Induced Enhancement of Cell-Mediated Immunity. Annals of the New York Academy of Sciences, 840: 359–372. doi: 10.1111/j.1749-6632.1998.tb09575.x
- Issue published online: 7 FEB 2006
- Article first published online: 7 FEB 2006
Abstract: We have demonstrated that acute stress induces a large-magnitude, rapid, and reversible redistribution of leukocytes from the blood to other compartments within the body. These changes in leukocyte distribution are mediated by adrenal stress hormones. Because the skin is one of the target organs of a stress-induced redistribution of leukocyes, we hypothesized that such a leukocyte redistribution could be one of the factors by which acute stress may enhance cutaneous immune function. This hypothesis was tested by examining the effects of acute stress on cutaneous delayed-type hypersensitivity (DTH). DTH reactions are antigen-specific, cell-mediated immune responses that, depending on the antigen involved, mediate beneficial (resistance to viruses, bacteria, and fungi) or harmful (allergic dermatitis, autoimmunity) aspects of immune function. DTH was induced by challenging the pinnae of previously sensitized rats with 2,4-dinitro-1-fluorobenzene (DNFB). Experiments showed that acute stress administered immediately before the introduction of an antigenic challenge significantly enhances a cutaneous DTH response. In contrast, chronic stress suppresses cutaneous DTH. These results demonstrate a bidirectional relationship between stress and immune function, such that acute stress enhances, while chronic stress suppresses, an important class of immune responses in vivo. They also suggest that stress-induced alterations in lymphocyte redeployment within the body may play an important role in mediating these bidirectional effects of stress on cell-mediated immunity.