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Clinical Depression and Regulation of the Inflammatory Response During Acute Stress

From the Department of Psychology, University of British Columbia, Vancouver, British Columbia, Canada (G.E.M., C.S.) and the Department of Psychology, Technical University of Dresden, Dresden, Germany (N.R., C.K.)

View larger version (26K): [in a new window]   Figure 1. Mean IC50 values for IL-6 and TNF- during stressor as a function of diagnosis (error bars represent standard error of mean). This figure shows that depression moderates the impact of acute stress on the immune system’s sensitivity to the anti-inflammatory properties of glucocorticoids. This measure reflects the capacity of dexamethasone to inhibit the in vitro production of IL-6 and TNF-. Depressed subjects began the session with higher sensitivity to dexamethasone’s anti-inflammatory properties than control subjects. Following exposure to the stressor protocol, however, sensitivity declined among depressed subjects and increased among control subjects. Sensitivity returned to baseline by the end of the recovery period for both cytokines.