Skin: what function does it serve?

The skin serves as the body’s first line of defence against the external environment. Its barrier function relies on a multi-layered organisation of cutaneous tissue, where each component helps to restrict the penetration of foreign substances and to prevent dehydration. The stratum corneum, composed of corneocytes embedded in a lipid matrix (ceramides, cholesterol, free fatty acids), acts as a semi-permeable physical barrier. This “brick and mortar” architecture minimises transepidermal water loss and blocks the entry of pathogens or irritants.

In addition to its mechanical role, the skin also fulfils a chemical barrier function. The hydrolipidic film, present on the surface of the epidermis, is slightly acidic (pH between 4.5 and 5.5), which limits microbial proliferation and stabilises the skin microbiome. The sebaceous glands and sweat glands actively participate by releasing fatty acids, salts and antimicrobial peptides, such as defensins or cathelicidin, capable of acting against pathogenic bacteria. This chemical environment of the skin contributes to preventing infections.

Finally, the skin possesses an integrated immunological barrier, composed of immunocompetent cells present as early as the superficial layers of the epidermis. The keratinocytes themselves participate in the immune response by releasing pro-inflammatory cytokines upon insult. Furthermore, Langerhans cells, macrophages and T lymphocytes ensure the recognition and elimination of foreign bodies.

The skin is a true immunological interface, housing a complex network of cells and mediators responsible for defending against pathogens while maintaining balance with the cutaneous microbiome. Keratinocytes and sebocytes actively participate in innate immunity through their recognition receptors, such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs). These sensors detect microbial patterns (lipopolysaccharides, peptidoglycans, bacterial or viral nucleic acids) and trigger the activation of T lymphocytes, immune cells capable of eliminating pathogens and tumour cells.

Skin immunity also relies on the production of antimicrobial peptides and lipids. Human β-defensins (hBD1-3) and the cathelicidin LL-37 modulate the immune response by recruiting macrophages, mast cells and dendritic cells. Other epithelial proteins, such as Small Proline Rich Proteins (SPRR), help limit bacterial colonisation, while sebaceous lipids, such as sapienic acid and linoleic acid, exert bactericidal activity by disrupting microbial membranes. These various mechanisms allow the skin to maintain a balanced flora and prevent pathogen proliferation.

Finally, the skin harbours a vast reservoir of resident immune cells, including Langerhans cells, the epidermal sentinels that capture antigens and activate memory T lymphocytes. The dermis also houses dendritic cells, macrophages, mast cells and regulatory T lymphocytes (Treg) which participate in limitation of inflammation. Resident memory T lymphocytes (Trm), estimated at over 20 billion in human skin, provide rapid local protection upon re-exposure to a pathogen.

The skin also plays a key role in sensory perception. Owing to its considerable density of nerve receptors, it captures a wide range of stimuli, whether tactile, thermal, painful or vibratory, and transmits these signals to the cerebral sensory cortex. This rapid communication enables the body to respond instantaneously, such as during a withdrawal reflex when exposed to a heat source. Certain regions, like the fingertips or lips, possess a particularly high concentration of nerve endings, granting them significant tactile sensitivity.

Skin sensory receptors are divided into encapsulated endings, such as Meissner, Pacinian or Ruffini corpuscles, and unencapsulated endings. The former, protected by a connective tissue capsule, detect pressure, vibrations and skin stretch. Free nerve endings, lacking any sheath, mediate pain perception, also known as nociception, and temperature perception, also known as thermoception, particularly in glabrous regions such as the palms of the hands or the soles of the feet.

The skin also contributes to the body’s thermal regulation, ensuring the maintenance of a stable internal temperature (≈ 37 °C) despite environmental fluctuations. This is made possible by the dense vascular network of the skin. When it is hot, cutaneous blood vessels dilate, increasing blood flow to the surface of the skin so that heat can dissipate. Sweating further complements this mechanism, as the evaporation of sweat at the epidermal surface cools the skin. Conversely, when temperatures drop, the blood vessels constrict to reduce surface blood flow and conserve internal heat, as do the arrector pili muscles, producing goose bumps.

Beyond these reflex mechanisms, the thermoregulation of the skin is governed by the autonomic nervous system and by hormonal mediators such as adrenaline or noradrenaline. Cutaneous thermoreceptors, sensitive to local temperature fluctuations, transmit signals to the hypothalamus, the body’s temperature-control centre. Thus, the skin acts as both a sensor and an effector: it detects thermal changes and initiates the necessary physiological responses to maintain homeostasis.

The skin can also be regarded as a peripheral neuroendocrine organ, capable of sensing, producing and responding to neural and hormonal signals. This function relies on a dense network of sensory and autonomic (sympathetic and parasympathetic) nerve fibres in close interaction with skin cells and the immune system. Nerves release various neuromediators, such as acetylcholine (ACh), noradrenaline, substance P or the calcitonin gene-related peptide (CGRP), which act on specific receptors located on the surface of keratinocytes, fibroblasts and immune cells. At the same time, skin cells express hormone receptors similar to those found in the brain and endocrine glands, allowing them to respond to systemic hormones such as cortisol or adrenaline.

These interactions modulate various functions, such as cell growth, wound healing, vasodilation and also the inflammatory response.

The sympathetic nervous system plays a major role in regulating microcirculation and stress responses via the release of noradrenaline, which controls vasoconstriction and sweat production. In contrast, the parasympathetic system, via acetylcholine, promotes processes of cellular regeneration and relaxation, contributing to the maintenance of cutaneous homeostasis. These systems are modulated by the hypothalamic–pituitary–adrenal axis which, in response to stress, induces cortisol production. Cortisol exerts a short-term anti-inflammatory effect but can impair barrier function and skin repair when produced chronically. The skin thus maintains a constant dialogue with the central nervous and endocrine systems, forming a bidirectional network that allows adaptation of skin responses to stimuli external (UV, heat, microbiota) and internal (stress, emotions).

The skin is also widely recognised for its metabolic role, particularly in ensuring the synthesis of vitamin D. Under the action of UVB rays, 7-dehydrocholesterol in the epidermis is converted into previtamin D3, which is then transformed into active vitamin D3 by the liver and kidneys. The latter contributes to the regulation of calcium and phosphorus, and thus to bone health, but also influences other metabolic functions, such as modulation of the immune response and support of muscle function. The skin’s capacity to produce vitamin D depends on several factors, including age, the phototype, sun exposure and the integrity of the skin barrier.

Note : Contrary to a widespread misconception, sunscreen does not cause a vitamin D deficiency.

The skin is one of the first aspects that others notice about us, making it a true mirror of our health. It not only serves as a physical barrier against external aggressions, but also reflects our internal states, whether physiological or psychological. Visible skin conditions, such as acne, eczema, psoriasis, as well as temporary changes linked to stress, fatigue or hormonal imbalances, can reveal disturbances within the body, whether immunological, endocrine or psychological. These manifestations have a direct impact on how a person is perceived socially: they can alter daily interactions, influence self-confidence and affect the subjective perception of one’s appearance.

The skin thus plays a central role, both biologically and socially.

• CHRISTOPHERS E. & al. What is the 'true' function of skin? Experimental Dermatology (2002).

• Société Française de Dermatologie. Structure de la peau. Annales de Dermatologie et de Vénéréologie (2005).

• STEINHOFF M. & al. Neuronal control of skin function: The skin as a neuroimmunoendocrine organ. Physiological Reviews (2006).

• WEBB A. R. & al. Who, what, where and when – Influences on cutaneous vitamin D synthesis. Progress in Biophysics and Molecular Biology (2006).

• CARLSBERG C. Nutrigenomics of vitamin D. Nutrients (2019).

• Thèse de Mazin AZIZ. Design and implementation of a sensing unit for tactile vision aid (theoretical background) (2020).

• SCHARSCHMIDT T. C. & al. Skin immunity: Dissecting the complex biology of our body’s outer barrier. Mucosal Immunology (2022).

• CALAMITA G. & al. Aquaporins are one of the critical factors in the disruption of the skin barrier in inflammatory skin diseases. International Journal of Molecular Sciences (IJMS) (2022).

• ARBISER J. A. & al. Skin barrier function: The interplay of physical, chemical, and immunologic properties. Cells (2023).

• SHARMA S. & al. Anatomy, skin (integument), epidermis. StatPearls (2024).