Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are autoimmune disorders with a preponderance in females. RA and SLE differ in their response to sex hormones. Disease development of RA is mitigated by estrogen and pregnancy whereas SLE tends to flare during pregnancy and in response to estrogen. Pregnancy improves the symptoms of RA in about 75% of pregnant patients, but relapses within six months postpartum in 90% of cases. RA is regarded as a T cell-mediated and TH1 immune response-driven disease. Pregnancy induces a shift from TH1 to TH2 immune response, increasing the anti-inflammatory cytokines IL-4 and IL-10, which may contribute to gestational amelioration of RA. Prospective studies of SLE pregnancies indicate that about 50% of patients experience a flare, however, with no permanent aggravation of the disease. Lupus nephritis, presence of antiphospholipid antibodies, and a previous history of pregnancy loss increase the risk of complications during pregnancy and fetal loss. The marked increase of estrogen and progesterone during pregnancy seems to enhance some of the manifestations of SLE. The shift to a TH2 immune response may trigger SLE manifestations that are dependent on humoral immune responses such as lupus nephritis. Another factor stimulating immune responses is the pituitary hormone prolactin, which has been found elevated in SLE patients of both sexes and correlated to disease activity in several studies. The hyperprolactinemia of lactation seems to influence postpartum behavior of SLE as well as RA.