Depression-related disturbances in mitogen-induced lymphocyte responses and interleukin-1 beta and soluble interleukin-2 receptor production.

In an attempt to delineate the pathophysiology underpinning the previously reported blunted lymphocyte responses to mitogenic stimulation in depressed patients, we measured the following immune variables in 28 depressives and 10 healthy controls: pre- and postdexamethasone (1 mg orally) lymphocyte responses to various mitogens, such as phytohaemagglutinin (PHA), and the PHA-induced accumulation of interleukin-1 beta (Il-1 beta) and soluble interleukin-2-receptors (sIl-2Rs) in culture supernatants. In the predexamethasone state, we found significantly more mitogen-stimulated blastogenesis in minor depressives vs healthy controls and major depressives. In depressed subjects there was a significant inverse relationship between the severity of illness and the mitogen-induced lymphocyte responses. Melancholics exhibited significantly more Il-1 beta accumulation in PHA culture supernatant than healthy controls. In healthy controls--but not in depressed patients--the sIl-2R accumulation perfectly reflects the magnitude of the PHA-induced lymphocyte stimulation. Dexamethasone administration significantly suppressed the lectin-induced blastogenesis and the Il-1 beta production rate in normal volunteers, whereas depressives exhibited dexamethasone nonsuppression in those factors. Healthy controls exhibited significantly less postdexamethasone blast transformation, Il-1 beta and sIl-2Rs accumulation in culture supernatant than the depressed patients.