Abstract
Immunoregulatory activity of type I interferons (IFNs) and estrogen is convergent in some cases of autoimmune disorders. The aim of our study was to determine whether a potent interaction of IFN and estradiol (E2) has an influence on immune response and estrogen receptor alpha (ER-α) expression in antigen-presenting cells in a model of experimental autoimmune orchitis (EAO). C3H/He/W male mice were immunized with testicular germ cells (TGCs) and orally treated with interferon tau (IFN-τ), E2, or both simultaneously. The delayed-type hypersensitivity reaction was intensified after the administration of either IFN-τ or E2, but their co-administration had no effect. IFN-τ treatment increased immunoglobulin G2a (IgG2a) and decreased IgG1 levels of TGC-specific antibodies, whereas E2 abolished the effects of the used cytokine. The total splenic cellularity and the number of spleen CD11c+MHC II+ and F4/80+MHC II− cells were increased after IFN-τ treatment, whereas E2 antagonized this effect. After IFN-τ administration the level of ER-α was significantly higher in F4/80+MHC II− cells, whereas E2 had no effect. However, the administration of E2 significantly reduced the ER-α level in F4/80+MHC II+ and CD11c+MHC II+ cells in comparison with the IFN-τ–treated groups. In the EAO model, the type I IFN and E2 cooperated at the general and cellular levels of immune response, but E2 treatment usually abolished the effects exerted by the cytokine.
Get full access to this article
View all access options for this article.
