Illuminating the Role of Vitamin A in Skin Innate Immunity and the Skin Microbiome: A Narrative Review

Abstract

Vitamin A is a fat-soluble vitamin that plays an important role in skin immunity. Deficiencies in Vitamin A have been linked to impaired immune response and increased susceptibility to skin infections and inflammatory skin disease. This narrative review summarizes recent primary evidence that elucidates the role of vitamin A and its derivatives on innate immune regulators through mechanisms that promote skin immunity and sustain the skin microbiome.

Keywords: innate immunity; retinoic acid; skin immunity; skin microbiome; vitamin A.

Figure 1

Role of vitamin A on skin innate immunity. Schematic diagram of the role of vitamin A on promoting toll-like receptor expression, mast cells, and Langerhans cell regulation and keratinocyte proliferation. Created with BioRender.

Figure 2

Wound-induced hair neogenesis. Skin injury stimulates non-coding dsRNA to activate TLR3 signaling, which triggers retinoic acid and mediates wound-induced hair neogenesis. Created with BioRender. Adapted from Kim et al. [21]. dsRNA, double-stranded RNA; TLR3, toll-like receptor 3.

Figure 3

Schematic diagram of RELMα and cathelicidin involvement in skin immunity and the skin microbiome. Dietary vitamin A triggers the transcription of the Retnla gene which encodes the RELMα antimicrobial protein. When expressed, RELMα kills bacterial species that colonize the skin, shapes the resident microbiota and reduces the viability of invading pathogens such as Streptococcus pyogenes to limit infection. All-trans retinoic acid stimulates transcription of cathelicidin. When expressed, cathelicidin potentiates the immune response against microbial infection. Created in BioRender; adapted from Harris et al. [2]. RELMα, Resistin-like molecule α; Retnla, Resistin-like alpha precursor; CYP, cytochrome P450 family; VDR, Vitamin D receptor; TLR, toll-like receptor.