Skin wounds and compromised wound healing are major concerns for the public. Although skin wound healing has been studied for decades, the molecular and cellular mechanisms behind the process are still not completely clear. The systemic responses to trauma involve the body’s inflammatory and immunomodulatory cellular and humoral networks. Studies over the years provided essential insights into a complex and dynamic immunity during the cutaneous wound healing process. This review will focus on innate cell populations involved in the initial phase of this orchestrated process, including innate cells from both the skin and the immune system.

Un des enjeux majeurs de ce XXI^esiècle est la lutte contre le vieillissement, défini comme un ensemble de mécanismes physiologiques altérant les capacités physiques et intellectuelles de l’organisme. Le vieillissement de la peau n’est qu’un trait visible de ce processus. Il est associé à des défauts de cicatrisation majeurs liés à l’altération des propriétés biomécaniques des cellules cutanées, essentiellement des fibroblastes dermiques. Le système immunitaire, autre composante clé du maintien de l’homéostasie cutanée et du bon déroulement de la cicatrisation des plaies, subit aussi les effets du temps : l’immunosénescence cutanée consécutive limiterait la réponse anti-infectieuse et vaccinale, tout en favorisant un environnement pro-tumoral. Les principales atteintes cutanées dues au vieillissement, que celui-ci soit intrinsèque ou extrinsèque, seront détaillées avant d’énumérer les stratégies anti-âges efficaces pour lutter contre les stigmates dermiques et épidermiques liées à l’âge.

Background Male androgenetic alopecia (AGA) is the most common form of hair loss in men. It is characterized by a distinct pattern of progressive hair loss starting from the frontal area and the vertex of the scalp. Although several genetic risk loci have been identified, relevant genes for AGA remain to be defined. Objectives To identify biomarkers associated with AGA. Methods Molecular biomarkers associated with premature AGA were identified through gene expression analysis using cDNA generated from scalp vertex biopsies of hairless or bald men with premature AGA, and healthy volunteers. Results This monocentric study reveals that genes encoding mast cell granule enzymes, inflammatory mediators and immunoglobulin‐associated immune mediators were significantly overexpressed in AGA. In contrast, underexpressed genes appear to be associated with the Wnt/β‐catenin and bone morphogenic protein/transforming growth factor‐β signalling pathways. Although involvement of these pathways in hair follicle regeneration is well described, functional interpretation of the transcriptomic data highlights different events that account for their inhibition. In particular, one of these events depends on the dysregulated expression of proopiomelanocortin, as confirmed by polymerase chain reaction and immunohistochemistry. In addition, lower expression of CYP27B1 in patients with AGA supports the notion that changes in vitamin D metabolism contributes to hair loss. Conclusions This study provides compelling evidence for distinct molecular events contributing to alopecia that may pave the way for new therapeutic approaches.