Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by T helper 2 cell (Th2)-shifted abnormal immunity, skin barrier impairment, and pruritus. The prevalence of AD in childhood is slightly higher in boys than in girls; after puberty, the sexual difference is reversed. The female preponderance in all generations exists in intrinsic AD with enhanced Th1 activity and nickel allergy, lacking increased serum IgE or filaggrin mutation. AD is often deteriorated before menstruation. We review the effects of sex hormones on immune responses and skin permeability barrier and propose possible hypotheses for the above phenomena. After puberty, the immune responses of patients are remarkably influenced by sex hormones. Estrogen and progesterone enhance the activities of Th2/regulatory T cell (Treg) but suppress Th1/Th17. Androgens suppress Th1/Th2/Th17 and induce Treg. The skin permeability barrier is fortified by estrogen but is impaired by progesterone and androgens. Dehydroepiandrosterone suppresses Th2 but enhances Th1. The amount of steroid sulfatase converting dehydroepiandrosterone sulfate to dehydroepiandrosterone is higher in women than in men, and thus, women might be more susceptible to the influence of dehydroepiandrosterone. The balance of modulatory effects of sex hormones on immune responses and skin barrier might regulate the course of AD.
Highlights
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by T helper 2 cell (Th2)-shifted abnormal immunity, skin barrier impairment, and pruritus (Figure 1) [1,2,3]
Tight junctions (TJs) are dysfunctional in AD: the levels of zonula occludens 1 were decreased in the non-lesional sites of AD, and the levels of zonula occludens 1 and claudin-1 were decreased in the lesional sites relative to the levels in skin from healthy subjects [4]
We firstly review the previous studies regarding the regulatory effects of sex hormonal regulation in the generation-dependent sexual difference in the prevalence of extrinsic AD, hormones on the immune responses and skin barrier
Summary
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by T helper 2 cell (Th2)-shifted abnormal immunity, skin barrier impairment, and pruritus (Figure 1) [1,2,3]. Sex Reprinted hormonesfrom might modulate the course of AD in the context png This file is licensed the of immune responses, skin barrier, or pruritus. We firstly review the previous studies regarding the regulatory effects of sex hormonal regulation in the generation-dependent sexual difference in the prevalence of extrinsic AD, hormones on the immune responses and skin barrier. In adolescents and adults, Th1 activities are higher in men than in neration-dependent hormonal regulation sexual in the difference generation-dependent inpreponderance the prevalence sexual ofintrinsic difference extrinsic Indeterioration this the article, previous we studies firstly regarding review the the previous regulatory studies effects of sex the regulato nsic female of intrinsic deterioration. Produced in the adrenal cortex enhances hormones on the immune responses hormones and on skin the immune barrier
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