Alterations to the immune status of the pregnant woman are necessary to allow mothers to tolerate genetically different fetal tissues during pregnancy. These alterations lead to impaired cell-mediated immunity with increased susceptibility to certain infections such as tuberculosis. During pregnancy, the maternal immune system also shows a relative bias toward T helper type 2 immunity. Several inflammatory dermatoses are either unique to pregnancy or altered by the pregnant state. Immunologists are now beginning to understand the various factors that contribute to the maternal immune tolerance and, in particular, the role of classic (human leukocyte antigen [HLA]-A, HLA-B, HLA-C, and HLA-D) and non-classic (HLA-E, HLA-F, and HLA-G) major histocompatability antigens in this process. Human leukocyte antigen-G, in particular, seems to be important in protecting HLA mismatched tissue from the innate immune system, and investigation of HLA-G expression may help to explain how pregnancy affects inflammatory skin disease. Immunologists are now beginning to understand the alterations to the immune status of the pregnant woman that are necessary to allow mothers to tolerate genetically different fetal tissues during pregnancy. These alterations may help to explain how pregnancy effects inflammatory skin disease.