{Reference Type}: Journal Article
{Title}: Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis.
{Author}: Beck LA;Cork MJ;Amagai M;De Benedetto A;Kabashima K;Hamilton JD;Rossi AB;
{Journal}: JID Innov
{Volume}: 2
{Issue}: 5
{Year}: Sep 2022
暂无{DOI}: 10.1016/j.xjidi.2022.100131
{Abstract}: Skin barrier dysfunction, a defining feature of atopic dermatitis (AD), arises from multiple interacting systems. In AD, skin inflammation is caused by host-environment interactions involving keratinocytes as well as tissue-resident immune cells such as type 2 innate lymphoid cells, basophils, mast cells, and T helper type 2 cells, which produce type 2 cytokines, including IL-4, IL-5, IL-13, and IL-31. Type 2 inflammation broadly impacts the expression of genes relevant for barrier function, such as intracellular structural proteins, extracellular lipids, and junctional proteins, and enhances Staphylococcus aureus skin colonization. Systemic anti‒type 2 inflammation therapies may improve dysfunctional skin barrier in AD.