![]() ![]() In previous years, retinoids were found to contribute to LC maturation. ![]() Langerhans cells (LCs) are among the first dendritic cells to encounter microbial antigens. These cells are present in three subtypes: dermal dendritic cells, plasmacytoid dendritic cells and langerhans cells, which are the main DC subset in the epidermis. Retinoic Acid and Dendritic Cellsĭendritic cells are APCs that recognize external antigens and present them to naïve T cells. As there is no unified understanding that explains the effect of RA on keratinocyte development, a multicomponent mechanism may best explain the therapeutic success of retinoids in treatment of hyperkeratotic skin conditions. A few in vitro and in vivo studies have shown that retinoids modulate epidermal proliferation by exerting an anti-proliferative effect on keratinocytes through modulation of keratinocyte differentiation, tyrosine kinase expression and posttranslational processing of keratinocyte proteins. There is limited understanding of the mechanism by which retinoids regulate keratinocyte cell proliferation. It has been recognized that both vitamin A deficiency and excess can lead to abnormal epithelial keratinization as seen in acne vulgaris and psoriasis. The downstream signaling that results from the interaction between PRR and pathogen-association molecular patterns (PAMPs) leads to the release of proinflammatory cytokines that modulate the immune response. Keratinocytes are epithelial cells of the skin that express PRRs that activate the immune response when exposed to pathogens. The observation that TLR3 triggers RA synthesis and signaling to promote regeneration also implies that combining TLR3 agonists with RA could have therapeutic benefits in skin and hair regeneration. ![]() Thus, removal of TLR3 in the Tlr3 −/− mouse model abrogates RA production and hair follicle regeneration. show in mice and human keratinocytes that dsRNA induces intrinsic RA synthesis in a TLR3-dependent manner. TLR3 induces RA synthesis and signaling, which in turn promotes follicular hair regeneration. Emerging evidence suggests that WIHN requires both TLR3 and RA. It has previously been shown that damaged skin activates TLR3 and induces follicular regeneration through a process known as wound-induced hair neogenesis (WIHN) ( Figure 2). In skin, dsRNA that can activate TLR3 is generated by both skin damage and live viruses. The ligand for TLR3 is double-stranded RNA (dsRNA). In the skin, TLR2 and TLR3 biology is dependent on retinoic acid. Vitamin A, Retinoids, and the Skin’s Innate Immune Response A few key scientific studies published prior to 2005 were also included to provide a historical context to the evolving role of vitamin A on skin innate immunity and the skin microbiome. Scientific studies published between 20 in the databases of PubMed and Google Scholar were identified using the specific search terms ‘’vitamin A and skin innate immunity’’, ‘’retinoic acid and skin innate immunity’’, ‘’vitamin A and skin microbiome’’, ‘’retinoic acid and skin microbiome’’ and ‘’vitamin A and skin inflammation’’. In this review, we survey current knowledge on the role of vitamin A and its metabolite, retinoic acid, in skin innate immunity and the skin microbiome through examining primary animal and human studies. There is increasing evidence in the literature of the essential role of vitamin A and its derivatives in skin immunity. These defense strategies are in part mediated by nutrients that influence the gene expression of anti-microbial proteins and molecules that enhance skin immunity. The skin functions as a barrier against diverse microbial communities through a variety of immune defense strategies. The skin is the largest epithelial organ and acts as an essential barrier between internal organs and the outer microbial world. ![]()
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