topic dermatitis (AD), commonly called eczema, is a long-term, pruritic, inflammatory skin condition with a significant disease burden. 1 There is mounting evidence that persistent and new-onset AD is common in adults, 2,3 with prevalence estimates of AD in US adults ranging from 7% to 11%. 4,5 Research has documented the disease burden of AD, including its visible nature and the effect on itch and sleep, 1 but knowledge gaps remain. 6 Gaps include a poor understanding of symptoms other than itch, patients' treatment experience, and how different elements of burden of disease interact.As part of an externally led patient-focused drug development (PFDD) meeting with the US Food and Drug Administration (FDA), an online survey was conducted of people with AD to understand its association with quality of life and treatment preferences. In this study, we used data from adult par-ticipants with AD to describe its association with disease burden among adults. Methods Study Design and PopulationWe conducted an analysis of data collected from an externally led PFDD survey on AD (www.morethanskindeepeczema.org/). We followed American Association for Public Opinion Research (AAPOR) reporting guidelines. 7 The 32-item electronic survey was disseminated through patient advocacy groups, social media, and clinicians; as such, we could not calculate a response rate because there was no known denominator of potential respondents. The survey was administered between August 1, 2019, and October 11, 2019. IMPORTANCE Atopic dermatitis (AD) is long term and burdensome. Studies investigating disease burden in adults are limited in scope with gaps in understanding of the adult patient lived experience.OBJECTIVE To describe the multidimensional burden of AD among mainly US adults. DESIGN, SETTING, AND PARTICIPANTSThis survey study for an externally led patient-focused drug development meeting with the US Food and Drug Administration on adult patients with AD was conducted between

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burden do not reliably predict response to checkpoint inhibitor therapy. This is likely a multifactorial phenomenon comprised of varying host gene expression profiles, tumour molecular heterogeneity and unique tumour microenvironments. 6 There also exist differences in the anatomical domains of T lymphocytes, with skin-resident T cells being localized and active in the epidermis and high dermis compared with circulating T cells, which are present and functional in the peripheral blood, lymphatics and subdermal soft tissue. 7 Epidermal dysplasia and superficial cSCCs are likely able to evade recognition by circulating T cells, which are probably the group disinhibited by PD-1 inhibitor therapy. The early SCCs may essentially hide from the drug and the systemic immune response in the epidermis.As use of PD-1 inhibitors increases, we will have greater opportunity to observe this phenomenon of a possible epidermal-high dermal privileged tumour microenvironment. It will be useful to examine the impact of T-cell recruitment factors, both genetically determined host drug response and tumour specific, and functional differences in anatomical domains of T lymphocytes in the use of checkpoint inhibitors for keratinocyte carcinoma.

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