Abstract
Atopic dermatitis (AD) often presents more severely in African Americans (AAs) and with greater involvement of extensor areas. To investigate immune signatures of AD in AAs with moderate to severe pruritus, lesional and non-lesional punch biopsies were taken from AA patients along with age-, race-, and sex-matched controls. Histology of lesional skin showed psoriasiform dermatitis and spongiotic dermatitis, suggesting both Th2 and Th17 activity. Gene Set Variation Analysis showed upregulation of Th2 and Th17 pathways in both lesional versus non-lesional and lesional versus control (p < 0.01), while Th1 and Th22 upregulation were observed in lesional versus control (p < 0.05). Evidence for a broad immune signature also was supported by upregulated Th1 and Th22 pathways, and clinically may represent greater severity of AD in AA. Furthermore, population-level analysis of data from TriNetX, a global federated health research network, revealed that AA AD patients had higher values for CRP, ferritin, and blood eosinophils compared to age-, sex-, and race-matched controls as well as white AD patients, suggesting broad systemic inflammation. Therefore, AA AD patients may feature broader immune activation than previously thought and may derive benefit from systemic immunomodulating therapies that modulate key drivers of multiple immune pathways.
Highlights
Atopic dermatitis (AD) is a complex, inflammatory skin disease that presents with a wide range of endotypes underlying differences in disease p resentation[1,2,3,4]
hematoxylin and eosin (H&E) stained tissue samples for lesional and non-lesional AD skin are shown in Fig. 1; patterns of psoriasiform and spongiotic dermatitis are observed in lesional AD skin
Atopic dermatitis is traditionally associated with predominant Th2 polarization, with certain disease subtypes thought to be partially attributed to differential modulation of other immune pathways[27]
Summary
Atopic dermatitis (AD) is a complex, inflammatory skin disease that presents with a wide range of endotypes underlying differences in disease p resentation[1,2,3,4]. With the heterogeneity present in the clinical presentation of AD, additional studies are needed to better understand the molecular differences responsible for these unique clinical endotypes, especially in AA patients who are disproportionately affected by AD but are generally understudied. AD is thought to be primarily Th2-driven, recent studies have suggested that there are disease subtypes with distinct cytokine signatures. These studies have largely been conducted in European American adults and large gaps remain in the understanding of AD in AA patients at the molecular level. We hypothesized that atopic dermatitis in AA individuals would demonstrate broad cutaneous immune activation, including the Th2 and Th17 axes, given their more hyperkeratotic and lichenified phenotype
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