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Summary  Langerhans’ cells ( LC ) play pivotal roles in skin immune responses, linking innate and adaptive immunity. In aged skin there are fewer  LC  and migration is impaired compared with young skin. These changes may contribute to declining skin immunity in the elderly, including increased skin infections and skin cancer. Interleukin‐1 β  ( IL ‐1 β ) and tumour necrosis factor‐ α  ( TNF ‐ α ) are mandatory signals for  LC  migration and previous studies suggest that  IL ‐1 β  signalling may be dysregulated in aged skin. Therefore, we sought to explore the mechanisms underlying these phenomena. In skin biopsies of photoprotected young (< 30 years) and aged (> 70 years) human skin  ex vivo , we assessed the impact of trauma, and mandatory  LC  mobilizing signals on  LC  migration and gene expression. Biopsy‐related trauma induced  LC  migration from young epidermis, whereas in aged skin, migration was greatly reduced. Interleukin‐1 β  treatment restored  LC  migration in aged epidermis whereas  TNF ‐ α  was without effect. In uncultured, aged skin  IL ‐1 β  gene expression was lower compared with young skin; following culture,  IL ‐1 β  mRNA  remained lower in aged skin under control and  TNF ‐ α  conditions but was elevated after culture with  IL ‐1 β . Interleukin‐1 receptor type 2 (  IL 1R2 ) gene expression was significantly increased in aged, but not young skin, after cytokine treatment. Keratinocyte‐derived factors secreted from young and aged primary cells did not restore or inhibit  LC  migration from aged and young epidermis, respectively. These data suggest that in aged skin,  IL ‐1 β  signalling is diminished due to altered expression of   IL 1B  and decoy receptor gene   IL 1R2 .

Lower levels of interleukin‐1 β gene expression are associated with impaired Langerhans’ cell migration in aged human skin