A Review of the Clinical and Immunologic Effects of Estrogen on Atopic Dermatitis

Abstract

One of the most important immunologic phenomena in pregnancy is a shift from T-helper 1 (Th1) to T-helper 2 (Th2) immunity. As a result, pregnancy is associated with an exacerbation of Th2 mediated diseases such as systemic lupus erythematosis, atopic dermatitis, and forms of pemphigus such as pemphigus vulgaris. To summarize the clinical and immunologic effects of estrogen as they relate to atopic dermatitis, we performed an English-language PubMed search of articles combining key terms including "atopic dermatitis," "atopic eruption of pregnancy," "estrogen," and "pregnancy." Estrogen appears to cause Th2 polarization and subsequent increase in Th2 cytokines. Pregnant women with atopic disease have greater numbers of Th2 cells producing IL-4 and IFN-gamma cytokines, and a decrease in the Th1 chemokine ratio. Effects of estrogen on Th17 cells vary depending on cell type. Estrogen stimulates mast cell proliferation and promotes allergic sensitization. Overall, atopic dermatitis tends to worsen during pregnancy, at least in part due to the effects of estrogen on the immune system. New advances in therapies will require an increased understanding of the immunopathology of AD, some of which may be learned by studying its unique course in pregnancy.