THE EFFECTS OF IRON-DEFICIENCY AND IRON OVERLOAD ON CELL-MEDIATED-IMMUNITY IN THE MOUSE

The influence of Fe status on cell-mediated immunity was studied in we anling mice fed on Fe-deficient (7 mg Fe/kg), Fe-sufficient (120 mg Fe /kg) and high-Fe (3000 or 5000 mg Fe/kg) diets for 7 weeks. The contac t sensitivity (CS) response to dinitrofluorobenzene (DNFB), the in viv o delayed-type hypersensitivity (DTH) response to sheep erythrocytes ( SRBC) and the ability of primed spleen cells to transfer DTH response to naive normal mice were suppressed in mice consuming the Fe-deficien t diet. High-Fe diets (3000 or 5000 mg Fe/kg) selectively suppressed t he CS response to DNFB, but the DTH response to SRBC or the transfer o f DTH response by primed spleen cells to naive normal mice remained no rmal. Spleen cell functions associated with the expression of class II major histocompatibility (MHC) surface antigens, concanavalin A-induc ed interleukin-2 (IL-2) secretion or the antigen-presenting cell (APC) ability to stimulate antigen-dependent proliferation of an SRBC-speci fic helper T-lymphocyte clone were not altered by Fe status, However, consistent with the suppressed DTH response in the Fe-deficient mice w as the suppressed concanavalin A-induced T-lymphocyte blastogenesis an d the interferon-gamma (INF-gamma) production by spleen cells from mic e fed on the Fe-deficient diet. Spleen cells from mice fed on excess l evels of Fe in the diet secreted less INF-gamma than the control mice, although T-lymphocyte proliferation remained unaffected. Suppression of the cellular immune response associated with Fe deficiency may be r elated in part to impaired T-lymphocyte proliferation and INF-gamma se cretion rather than to deficits in IL-2 secretion or APC function.