Inhibition of 2,4-dinitrofluorobenzene-induced contact hypersensitivity reaction by antidepressant drugs

Background: contact hypersensitivity (chs) induced by a topical application of hapten - 2,4-dinitrofluorobenzene (dnfb),is a t cytotoxic (tc)1-cell-mediated antigen-specific type of skin inflammation. recently,it has been shown that antidepressant drugs inhibit the t helper (th)1-mediated chs reaction induced by picryl chloride. the aim of present study was to establish the effect of two-week desipramine or fluoxetine administration on the chs reaction induced by dnfb. methods: balb/c (h-2d) male mice were divided into six groups: 1) vehicle-treated negative control group; 2) desipramine-treated negative control group; 3) fluoxetine-treated negative control group; 4) vehicle-treated dnfb group (positive control group); 5) desipramine-treated dnfb group; 6) fluoxetine-treated dnfb group. t lymphocytes proliferation was determined by incorporation of [3h]-thymidine to dna of concanavalin a stimulated cells. elisa test was used for estimation of cytokines production. results: the antidepressants significantly suppressed the chs reaction mediated by tc1 cells: desipramine by 55% and fluoxetine by 54% compared to the positive control. moreover,the antidepressants decreased the proliferative activity of splenocytes and the ability of splenocytes to produce interleukin (il)-6 and interferon (ifn)-g and increased il-10 production by the lymph node (ln) cells of dnfb-treated mice. conclusion: the results of the present study show that the tc1-dependent reactivity to dnfb is significantly suppressed by antidepressant drugs,which suggests their inhibitory effect on tc1 mediated immunity.copyright © 2013 by institute of pharmacology polish academy of sciences.