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There is considerable evidence that the sympathetic nervous system influences the immune response via activation and modulation of β2-adrenergic receptors (β2R). Furthermore, it has been suggested that stress has effects on the sympathetic nervous system. In the present study, we analyzed the influence of catecholamines on the reactivity of lymphocytes from mice exposed to a chronic mild stress (CMS) model of depression (CMS-animals). The effects of the CMS treatment on catecholamine and corticosterone levels and on β2R lymphoid expression were also assessed. For this purpose, animals were subjected to CMS for 8 weeks. Results showed that catecholamines (epinephrine and norepinephrine) exert an inhibitory effect on mitogen-induced normal T-cell proliferation and a stimulatory effect on normal B-cell proliferation in response to selective B lymphocyte mitogens. Specific β- and β2-antagonists abolished these effects. Lymphocytes from mice subjected to CMS had an increased response to catecholamine-mediated inhibition or enhancement of proliferation in T and B cells, respectively. Moreover, a significant increase in β2R density was observed in animals under CMS compared to normal animals. This was accompanied by an increment in cyclic AMP production after β-adrenergic stimulation. On the other hand, neither catecholamine levels, determined in both urine and spleen samples, nor serum corticosterone levels showed significant variation between normal and CMS-animals. These findings demonstrate that chronic stress is associated with an increased sympathetic influence on the immune response and may suggest a mechanism through which chronic stress alters immunity.