Immune Activation In Major Depression

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The status of the immune system in major depression has been extensively studied over the last ten years and there is now some evidence that the acute episode of this illness may be accompanied by immune activation/acute phase response (Maes., 1993; Sluzewska et al., 1996b). The acute phase response (apr) is a response of the organism to disturbances of its homeostasis due to factors such as, infection, tissue injury, neoplastic growth or immunological disorders (Heinrich et al., 1990). Within this systemic reaction, that involves the endocrine, immunologic and metabolic system (Kushner and Mackiewicz., 1993), there are also behavioural changes, which are expressed as "sickness behaviour," characterised by psychomotor retardation, sleep disturbances, anorexia, anergy, and lethargy (Kent et al., 1992).

Changes in immune response in major depression include activation of the monocytic and T-lymphocytic arm of cell-mediated immunity (CMI), the apr, and autoimmune response.

An activation of the monocytic arm of CMI is suggested by:

— the production of an increased number of monocytes (Kronfol et al., 1989; Irwin et al., 1990; Maes et al., 1992c; Sluzewska et al., 1994c).

— increased plasma concentrations of IL-6, sIL-6R, IL-lß (Maes., 1993, 1995a; Sluzewska et al., 1995a, b, 1996b).

— increased plasma concentrations of neopterin (Dunbar et al., 1992; Maes et al., 1994b).

— increased plasma concentrations of prostaglandin E2 and tromboxan B2 (Lieb et al., 1993).

An activation of the T-lymphocytic arm of CMI is suggested by:

— increased number and percentage of T lymphocytes and T helper cells and increased T helper CD4+/T suppressor CD8+ ratio (Maes et al., 1992c, 1994a; Muller et al., 1993; Sluzewska et al., 1994c).

— T-cells activation as indicated by increased number and percentage of activated T-cells (CD25+) (Maes et al., 1992c, 1993; Sluzewska et al., 1994c).

— increased concentration of soluble interleukin-2-receptor (sIL-2R) and transferrin receptor (Trf) (Maes et al., 1995a; Nessberger et al., 1993; Schleifer et al., 1984; Sluzewska et al., 1996b).

— increased plasma concentrations of interferon (Maes et al., 1994b).

— increased plasma concentrations of soluble CD8 (sCD8) (Sluzewska et al., unpublished).

The presence of apr in major depression is suggested by:

— increased plasma concentrations of positive acute phase proteins (apps) such as:

alpha-l-acid glycoprotein (AGP) (Nemeroff et al., 1990; Healy et al., 1992;

Sluzewska et al.. 1993.1996a):

-1 antichymotrypsin (ACT) (Joyce et al., 1992; Sluzewska et al., 1995b); haptoglobin (Hp) (Joyce et al., 1992; Maes et al., 1992a, 1993); C-reactive protein (CRP) (Sluzewska et al., 1994c); celuroplasmin (Cp) (Maes et al., 1992a)

— downturn in negative acute phase proteins such as:

albumin (Maes et al., 1992a, 1995b; Joyce et al., 1992; Song et al. 1993; Sluzewska et al., 1997b) transferrin (Maes et al., 1992a)

The presence of autoimmune response in major depressive illness is suggested by:

— increased expression of antinuclear antibodies (Gastpar et al., 1981; Maes et al., 1991); antiphospholipid antibodies (Maes et al., 1991) and antibodies against serotonin and gangliosides (Schott et al., 1992; Sluzewska et al., 1997a).

During the last 15 years, a large number of studies have focused upon the ex vivo response of lymphocytes stimulated by mitogens. Most authors have observed decreased lymphocyte proliferation which is not due to decreased number of T lymphocytes but rather to the presence of immunosuppressive mechanisms such as: apr, decreased plasma levels of DPP IV (Maes et al., 1993), increased levels of sIL-2R and prostaglandins as well as Cortisol (Maes et al., 1989).

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