Pregnant females are susceptible to intracellular pathogens and are biased towards humoral rather than cell-mediated immunity. Since 7", 1 cymkines compromise pregnancy and 7", 2 cytokines are produced at the maternalfetal interface, we hypothesize that these T, 2 cytokines inhibit TH1 responses, improving fetal survival but impairing responses against some pathogens.

It is increasingly apparent that there is a bidirectional interaction between the maternal immune system and the reproductive system during pregnancy. Thus the maternal immune system can enhance or inhibit the development of the feto--placental unit, and the fetoplacental unit redirects maternal immunity away from cell-mediated immunity towards enhanced humoral responsiveness. Since Ts1 cytokines (interleukin 2 (IL-2), interferon gamma (IFN-~) and tumour necrosis factor (TNF)) are generally harmful to the maintenance of pregnancy, we put forward the hypothesis that the conceptus protects itself by secreting TH2 cytokines which downregulate the harmful cytokines. As a consequence~ the materna! immune system during pregnancy preferentially mounts TH2-biased responses, resulting m increased susceptibility to certain autoimmune diseases and intracellular infections.