A variety of hormonal and immunological alterations are induced by pregnancy in order to protect the semi-allogeneic fetus from rejection. Systemic effects of altered immunoregulation induced by pregnancy influence the activity of rheumatoid arthritis (RA) and other autoimmune diseases. Pregnancy induces improvement or even remission of disease activity in 75% of RA patients. This phenomenon has still not been explained, however, several attractive hypotheses related to the immunology of pregnancy emerge. Pregnancy polarizes the immune response towards a TH2 response, which may counterbalance the augmented TH1 response observed in RA. The increase of circulating inhibitors of proinflammatory cytokines occurring in pregnancy could act as a potent anti-inflammatory agent in joint inflammation. In what way the induction of T cell tolerance to fetal antigens or maternal-fetal HLA disparity modulates disease activity of RA has not been studied. The concept of regulatory T cells has been discussed in the context of pregnancy, but until now has not been substantiated by experimental data. In conclusion, pregnancy influences the signs and symptoms of RA, but not the underlying autoimmune process. It remains to be investigated if a single event like neutralisation of proinflammatory cytokines or an interplay between circulating and cellular mechanisms is the key to remission.