atopic dermatitis

[Journal of Immunology] Researchers performed a phenome-wide association study and reported that the T allele of GPR65-intronic single-nucleotide polymorphism rs8005161, which reduced GPR65 signaling, showed a significant association with atopic dermatitis, in addition to inflammatory bowel diseases and asthma, as previously reported.

[Genes & Immunity] The authors summarize the ongoing clinical studies that are targeting the microbiome in patients with skin disorders.

[Experimental Dermatology] The authors summarized the mechanisms of several common neuropeptides in atopic dermatitis (AD) and hypothesized that neuropeptides may be the novel potential targets in AD treatment.

[Cell Reports] Scientists found that Tmem79−/− mice spontaneously develop interleukin-17-producing T-cell-driven skin inflammation. Comparative skin microbiome analysis revealed that the disease activity index is negatively associated with S. cohnii.

[Journal of Autoimmunity] The authors evaluate the development of (autoreactive) T cells and their response to (auto)antigens, as well as the role of the peripheral tolerance in autoimmunity in the pathophysiology of atopic dermatitis (AD), including the unmet needs and gaps.

[Journal of Investigative Dermatology] Researchers investigated whether intracellular IL-33 is involved in IL-4/IL-13 function. In monolayer-culture and living skin equivalent, IL-4/IL-13 increased the expression of full-length IL-33 in the nucleus of keratinocytes by activating the MEK/ERK signaling pathway, which is necessary for the inhibition of differentiation markers filaggrin, loricrin, keratin1, and keratin 10.