Effects of subchronic exposure to diethylstilbestrol on humoral immune function in adult female (C3B6)F1 mice.

Adult female (C57BL/6 X C3H)F1 (B6C3F1) mice were treated with diethylstilbestrol for 14 days and assayed for the ability to produce antibody to a T-dependent antigen, a T-independent antigen, and to respond in vitro to stimulation by a polyclonal activator, bacterial lipopolysaccharide (LPS). No suppression of the in vivo antibody responses were observed. DES produced a subtle alteration in the response to the T-dependent antigen, sheep erythrocyte (sRBC), as treated groups maintained higher PFC values than vehicle groups after the peak day of the response. DES induced an enhanced response to the T-independent antigen, DNP-Ficoll. Spleen cells from DES-exposed animals were only marginally altered in their ability to produce antibody in vitro in response to LPS. Parallel experiments indicated a comparable reduction of LPS-induced blastogenesis. Serum immunoglobulin levels were determined following DES exposure, as a measure of baseline immunocompetence. DES only caused a reduction in the immunoglobulin M (IgM) isotype. DES exposure caused a significant enhancement of the activity of the reticuloendothelial (RES) system. Experiments were performed to assess the effects of enhanced RES function on concentrations of 51Cr labeled sRBC, which were optimal for antibody production. When sRBC were administered i.p., there was no effect on either the Ab response (as reported above) or on the number of sRBC localized in the spleen. In contrast, when sRBC were administered i.v., exposure to DES reduced (approximately 50%) both the Ab response and the number of sRBC localized in the spleen. Enhanced phagocytic function and alterations in antigen distribution must be considered in the interpretation of in vivo immune responses.