STRESS AND IMMUNITY - REVIEW OF STUDIES I N PSYCHONEUROIMMUNOLOGY

Citation
L. Fillion et al., STRESS AND IMMUNITY - REVIEW OF STUDIES I N PSYCHONEUROIMMUNOLOGY, Canadian psychology, 35(4), 1994, pp. 405-426
Citations number
133
Categorie Soggetti
Psychology
Journal title
ISSN journal
07085591
Volume
35
Issue
4
Year of publication
1994
Pages
405 - 426
Database
ISI
SICI code
0708-5591(1994)35:4<405:SAI-RO>2.0.ZU;2-K
Abstract
The thesis of a systemic link between stress and health has been aroun d for a long time. Psychoneuroimmunology (PNI) is a new interdisciplin ary field offering promising avenues for major developments in stress research. PNI focuses on the relationships between the nervous, endocr ine and immune systems. It aims, among other objectives, at providing an explanation for the role of psychosocial factors in individual resi stance to illnesses. Classic contributors to PNI have put forward four major propositions about the link between stress and immunity. They s tated that (1) psychosocial stressors caused an immunosuppressive resp onse, (2) this immunosuppressive response was observable under intense and enduring stress, (3) the immunosuppressive response led to increa sed vulnerability to illnesses, and (4) an improvement on stress state yielded to an increase in immune response. Recent studies either in t he laboratory or in the field have provided empirical evidence for the se hypotheses in humans. The objective of this paper is to review empi rical work relating immunity and stress as measured in terms of state, stressors or cognitive appraisal. Following a brief definition of psy chological stress in a transactional perspective, a presentation of th e immune system and its physiological interconnections, fifty studies in human PNI published since 1985 are introduced according to the type of contributions their design provided. Then a critical analysis is s uggested along with identification of common findings and finally a di scussion of the four propositions. Hypothesis 1 is supported in terms of immunomodulation while Hypothesis 2 is contradicted by the observat ion that short term laboratory stressors are sufficient to induce immu nomodulation. Not much evidence exist as yet to establish increased vu lnerability to illnesses, as stated by Hypothesis 3. Finally, clinical studies suggest possibilities to increase or restore immune responses .