engleski

Immune reactivity and PTSD

Immune system's primary goal, in the traditional view, is to discriminate between self and non-self. On the other hand, the Danger model (1) of immunity claims that immune system's principal driving force is protection against any endogenous danger that causes stress or damage. According to this model, immune system receives positive and negative alarm signals from an extended network of other bodily tissues. This fits very well in the picture of general stress response with tightly connected interactions between central nervous, endocrine and immune system. The systems communicate through common signalling molecules of neuropeptides, hormones, cytokines, and their cell receptors. The immune system is composed of lymphoid organs (the bone marrow, the thymus, the spleen, the lymph nodes) and specialised cells that recirculate between the organs by the blood or the lymph (lymphocytes, monocytes, granulocytes), or resides in the organs or tissues (macrophages, dendritic cells). The cells in these organs communicate through cell-to-cell contacts and diverse soluble mediators that regulate immune response (2). To assess the efficiency of the immune system, the cells have to be isolated from peripheral blood, and two kinds of immune assays are used. By enumerative assays, the number and proportion of different cell populations (and subpopulations) or their solubile products (antibodies, cytokines), can be quantified. The significance and interpretation of findings may be difficult and controversal, as they frequently reflect redistribution of cells between lymphoid organs. By functional assays, the activity of particular cell type can be assessed in vitro or ex vivo. Among the most basic lymphocyte functions are proliferation, cytokine production and cytototoxic activity. Phagocytic activities (ingestion, digestion, antibody dependent extracellular cytotoxicity) of monocytes and granulocytes are usually performed. Immunological studies in chronic stress are numerous (3-6), and it is widely believed that stressful experiences suppress immune functions. Investigations of immune status in PTSD has been scarce. Our results on war-related chronic stress (displaced persons, detainees from the concentration camp) and on combat-related PTSD (professional soldiers, war veterans) will be reviewed and discussed. The findings of increased numbers of effector cells (B, TC, NK lymphocytes), their activated subpopulations, and some of the main functions (spontaneous proliferation, NK-activity, inflammatory cytokines production) suggest an enhancement of the immune response in chronic stress.

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