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Abbreviations: TCA: tricyclic antidepressants. MAOI: monoamine oxydase inhibitors. SSRI: selective serotonin reuptake inhibitors.

Abbreviations: TCA: tricyclic antidepressants. MAOI: monoamine oxydase inhibitors. SSRI: selective serotonin reuptake inhibitors.

with tricyclic antidepressants, whereas it was normal before treatment. It should be noted that in this study, depression of mitogenesis was also observed after electroconvulsive therapy (Albrecht et al., 1985). The elevation of monocyte counts observed at the onset of a depressive episode decreased after six weeks of treatment with tricyclics, and this decrease was associated with clinical improvement (Seidel et al., 1996). In contrast, when monocyte functions, such as class II and CD14 antigens expression, TNF production and plasma IFNy, were found to be unaltered at the onset of depression, these functions remained normal after a 4-12 week moclobemide therapy (Landmann et al., 1997). It has also been reported that the increased plasma levels of IL-6 observed during acute depression was normalized after an 8-week period of fluoxetine treatment. However, this normalization was observed only in 6 out of 22 patients (Sluzewska, Rybakowski, Laciak, Mackiewicz, Sobieska, & Wiktorowicz, 1995a). As described previously, the use of cytokines to treat some diseases, such as IFN-ip for multiple sclerosis, could be associated with the onset of a depressive episode (Mohr et al., 1997). Antidepressant medication as well as psychotherapy improve adherence of patients to IFNp therapy (Mohr et al., 1997). It has been suggested that tricyclic antidepressants may be successful in alleviating the neuropsychiatrie disturbances induced by INFa therapy including depression (Goldman, 1994).

In a recent study in ten patients with major depression, a 4-week treatment with clomipramine, a tricyclic antidepressant, increased the production of IL-lp, IL-3, and to a lesser extent IL-2, by peripheral blood mononuclear cells in depressed patients presenting reduced cytokine production before treatment (Weizman et al., 1994). Cytokine production before and after drug treatment did not correlate with severity of depression as assessed by the Beck Depression Inventory (Weizman et al., 1994). In addition, lithium treatment induced in breast cancer patients an increase of TNFa production (Merendino, Mancuso, Tomasello, Gazzara, Cusumano, Chillemi, Spadaro, & Mesiti, 1994), and this increase could be confirmed in vitro. Furthermore, a preliminary report in a small group of homosexual men with HIV infection and major depression suggests that treatment with imipramine mght minimize the decline in T4 cell count (Rabkin & Harrison, 1990).

From these clinical studies, it is not possible to conclude whether antidepressants have a direct effect on the immune system or whether their putative immune effects result from improved mood. Further experiments, comparing the effects of antidepressants and other antidepressive therapy like psychotherapy or electroconvulsive therapy, would be necessary to answer this question.

4.2. Immune Effects of Antidepressants in Experimental Models

Investigation of the effects of antidepressant treatment on immune activity, and especially on cytokine production and/or central actions, is still in its infancy, and not much data are so far available (Table 2). In normal mice, chronic administration of maprotiline, a highly selective noradrenergic reuptake blocker, but not of desipramine, suppressed NK activity both in vivo and in vitro. Delayed hypersensitivity and T cell proliferation in vitro were not affected by this treatment, suggesting selectivity of the maprotiline effect (Eisen, Irwin, Quay, & Livnat, 1989). In another experiment, it was shown that, in mice, imipramine depressed delayed hypersensitivity to sheep erythrocytes when this antidepressant was injected i.p. as a single dose of 4 or 8mg/kg on the day of immunization or of challenge, or daily from immunization to challenge (Descotes, Tedone, & Evreux, 1985). In rats subjected to chronic mild stress model of depression, the enhanced proliferation of lymphocytes, as well as IL-1 and IL-2 production by stimulated splenic cells, were reversed by a chronic treatment with imipramine (Kubera, Symbirtsev, Basta-Kaim, Borycz, Roman, Papp, & Claesson,

Table 2. Effects of antidepressants on immune functions in laboratory animals

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