Pregnancy and pregnancy-associated hormones alter immune responses and disease pathogenesis.

During pregnancy, it is evolutionary advantageous for inflammatory immune
responses that might lead to fetal rejection to be reduced and anti-inflammatory 
responses that promote transfer of maternal antibodies to the fetus to be
increased. Hormones modulate the immunological shift that occurs during
pregnancy. Estrogens, including estradiol and estriol, progesterone, and
glucocorticoids increase over the course of pregnancy and affect transcriptional 
signaling of inflammatory immune responses at the maternal-fetal interface and
systemically. During pregnancy, the reduced activity of natural killer cells,
inflammatory macrophages, and helper T cell type 1 (Th1) cells and production of 
inflammatory cytokines, combined with the higher activity of regulatory T cells
and production of anti-inflammatory cytokines, affects disease pathogenesis. The 
severity of diseases caused by inflammatory responses (e.g., multiple sclerosis) 
is reduced and the severity of diseases that are mitigated by inflammatory
responses (e.g., influenza and malaria) is increased during pregnancy. For some
infectious diseases, elevated inflammatory responses that are necessary to
control and clear a pathogen have a negative consequence on the outcome of
pregnancy. The bidirectional interactions between hormones and the immune system 
contribute to both the outcome of pregnancy and female susceptibility to disease.