Several authors have show the occurrence of antinuclear, antiphospholipid and antiserotonin, antihistone, antibodies in depression (Villemain, 1988; Irwin et al., 1990; Maes et al., 1991; Schott et al., 1992). Some autoimmune disorders have been related to the induction of antihormone and anti-receptor antibodies (Cohen and Cook, 1986). We have recently reported the occurrence of antibodies against serotonin and gangliosides in major depressed patients (Sluzewska et al., 1997d). Antibodies against gangliosides have been shown to be part of the serotonin receptor complex (Fishman, 1988). Patients with major depression showed a significant antibody reactivity of IgG or IgM type to serotonin (55% of the patients) and to gangliosides (50% of the patients). In most patients the antibody against serotonin was associated with the antibody against gangliosides. 73% of the major depressed patients with antibodies against serotonin and 70% major depressed patients with gangliosides antibodies were TRD patients. Among 66% of the TRD patients studied, the antibodies against serotonin were present and in 58% of the cases the antibodies against gangliosides were present too. Patients with antibodies against serotonin and gangliosides showed more elevated levels of CRP, AGP, and ACT. They also presented different patterns of microhetero-geneity with higher values of AGP-RC (type I of glycosylation changes), elevated serum levels of IL-6, and decreased levels of serotonin in comparison to normal controls (Sluzewska et al., 1997d).
IL-6 may be involved in the production of autoantibodies which, in turn, could be an element of pathogenesis of autoimmune diseases (Cavallo et al., 1994). Antinuclear and antiphospholipid antibodies have already been found in depression (Maes et al., 1991). In addition, decrements of serum serotonin levels in major depression are express specifically in TRD; the frequent association of anti-serotonin and anti-gangliside antibodies, as well as the fact that gangliosides indicate the component of serotonin receptor complex (Fishman, 1988) allow us to speculate that these indicators may be anti-receptor antibodies. Since the concomitant presence of the apr was observed, it may be hypothesized that changes in the serotonin receptor system are related to the apr and that there is an immune (autoimmune) process in depression. Still, there is no evidence, referring to causation, of such a process. One may only speculate that the induction of antiserotonin and antiganglioside antibodies is the consequence of the viral infection or of the stress factors involved in the overproduction of cytokines (eg. IL-6); these factors appear to act within a regulary network, and biological outcome in infection are likely to be representative of the unique, as well as common, action of the "cascade" mediators (Balkweill and Burke, 1989; Balkweill, 1993). Although these immunological data are difficult to interpret, they appear to support the notion of an involvement of (auto) immunity in the pathogenesis of depression.
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