Type 2 inflammatory diseases in atopic dermatitis: A short review

Abstract

Type 2 inflammatory diseases are characterized by the dysregulation of the T helper (Th) 2 pathway, the prototype being atopic dermatitis (AD). The common inflammatory pathways, genetic risk factors, epidermal barrier dysfunction, parental atopy, and environmental factors are all associated with the codevelopment of type 2 inflammatory diseases in patients with AD. Acute skin barrier disruption leads to the production of both alarmin and dopamine, both of which promote Th2 skewing and mast cell activation, which then finally leads to inflammation, pruritus, and initiation of type 2 immune responses. Since AD is considered “starting point” for various other allergic diseases, its judicious management can help in decreasing the comorbidity posed by respiratory allergy and allergic rhinitis. This review discusses our current understanding of the type 2 inflammation in AD and highlights the nuances between the various type 2 inflammatory disorders. The article tends to focus on the fact that type 2 inflammatory diseases have a significant burden in patients with AD and it is far beyond the cutaneous manifestations and the “Atopic March.” There is an emphasis on early identification and an integrative approach in the treatment of AD in order to alleviate the overall disease morbidity. Type 2 immunity will be reviewed in the light of the prevailing as well as forthcoming targeted treatment options for AD and other related type 2 inflammatory disorders.