Inflammation is traditionally considered a defense response induced by infection or injury. However, inflammation can also be induced by tissue stress and malfunction in the absence of infection or overt tissue damage. Here we discuss the relationship between homeostasis, stress responses and inflammation. Stress responses have cell autonomous and cell extrinsic components, the latter contributing to tissue level adaptation to stress conditions. Inflammation can be thought of as the extreme end of a spectrum that ranges from homeostasis to stress response to bona fide inflammatory response. Inflammation can be triggered by two types of stimuli: extreme deviations of homeostasis or challenges that cause a disruption of homeostasis. This perspective may help to explain qualitative differences and functional outcomes of diverse inflammatory responses.

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For decades, treatment of atopic dermatitis (AD) has been limited to topical corticosteroids, topical calcineurin inhibitors, and for those with moderate-to-severe AD, phototherapy and systemic immunosuppressants.Despite medical need for more aggressive management, many patients are undertreated owing to concerns about the adverse effects and frequent laboratory monitoring associated with systemic immunosuppressants. Even adherence to topical regimens is threatened by caregiver phobia about the use of topical corticosteroids and calcineurin inhibitors.Of note, the following 2 targeted therapies have recently been approved by the US Food and Drug Administration for treatment of AD: topical crisaborole 2% ointment, a phosphodiesterase 4 inhibitor, and subcutaneously injected dupilumab, a monoclonal antibody targeting the interleukin-4 receptor.Given the recent advances in our understanding of AD pathogenesis, numerous topical and systemic targeted therapies are in development and likely to alter the landscape of therapeutic options for AD.

Atopic dermatitis (AD) and psoriasis are chronic inflammatory skin diseases associated with a significant cutaneous and systemic burden of disease as well as a poor health-related quality of life. Here, we review the complex pathophysiology of both AD and psoriasis and discuss the implications for treatment with current state-of-the-art and emerging topical and systemic therapies. Both AD and psoriasis are caused by a complex combination of immune dysregulation, skin-barrier disruption, genetic factors, and environmental influences. Previous treatments for both diseases were limited to anti-inflammatory agents that broadly suppress inflammation. Emerging insights into relevant pathways, including recognition of the role of T-helper type 2 driven inflammation in AD and T-helper 1 and 17 driven inflammation in psoriasis, have led to a therapeutic revolution. There are a number of novel treatment options available for AD and psoriasis with many more currently under investigation.