Oestradiol- and testosterone-mediated effects on the immune system in normal and autoimmune mice are genetically linked and inherited as dominant traits.

Abstract

The influence of sex steroids on cutaneous delayed-type hypersensitivity (DTH) and antibody responses to oxazolone (OXA) in autoimmune and normal mouse strains has been investigated. The results show that: (i) treatment with 17 beta-oestradiol (E2) suppresses DTH responses and stimulates antibody responses in MRL, B6 and C3H mice, suppresses DTH in DBA/1 mice, while having no effects on DTH or antibody responses in BALB/c and NFR/N mice. (ii) Treatment with testosterone suppresses the antibody response in all studied strains (MRL, B6, BALB/c and DBA/1) while down-regulating the DTH response only in MRL and B6 but not in BALB/c or DBA/1. (iii) Neither the lympho-proliferative (lpr) gene, which accelerates autoimmune disease, nor the H-2 genes seem to be directly related to the effects of sex hormones on the immune system. (iv) Susceptibility to oestrogen- and testosterone-mediated suppression of DTH but not oestrogen-mediated enhancement of antibody response are inherited as dominant traits. The results are discussed in the context of certain autoimmune diseases known to be influenced by sex hormone manipulations.