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Review
. 2017:2017:5095293.
doi: 10.1155/2017/5095293. Epub 2017 Oct 18.

Skin Immune Landscape: Inside and Outside the Organism

Florence Abdallah  1 , Lily Mijouin  2 , Chantal Pichon  1   3
Affiliations
Review

Skin Immune Landscape: Inside and Outside the Organism

Florence Abdallah et al. Mediators Inflamm. 2017.

Abstract

The skin is an essential organ to the human body protecting it from external aggressions and pathogens. Over the years, the skin was proven to have a crucial immunological role, not only being a passive protective barrier but a network of effector cells and molecular mediators that constitute a highly sophisticated compound known as the "skin immune system" (SIS). Studies of skin immune sentinels provided essential insights of a complex and dynamic immunity, which was achieved through interaction between the external and internal cutaneous compartments. In fact, the skin surface is cohabited by microorganisms recognized as skin microbiota that live in complete harmony with the immune sentinels and contribute to the epithelial barrier reinforcement. However, under stress, the symbiotic relationship changes into a dysbiotic one resulting in skin disorders. Hence, the skin microbiota may have either positive or negative influence on the immune system. This review aims at providing basic background information on the cutaneous immune system from major cellular and molecular players and the impact of its microbiota on the well-coordinated immune responses in host defense.

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Figures

Figure 1
Figure 1
Illustration of skin microbiota interaction with the SIS. The alliance between skin immunity and local flora allows protection against external pathogens and maintenance of tolerance to resident microorganisms, simultaneously. In a healthy state, resident bacteria such as S. epidermidis are able to contain S. aureus pathogenicity. Moreover, S. epidermidis was shown to be required for the production of IL-17 and IFN-γ by T cells inhibiting L. major growth. However, altered resident microbial communities or local expansion of some members of skin microbiota with harmful potential alters this alliance. S. aureus is able to produce δ toxins that trigger local allergic responses in skin resulting in TH2 inflammatory immune response. Adapted from [157].
Figure 2
Figure 2
Skin anatomy and cellular constituents. The protection of the body from the external environment is provided by the multilayered structure as well as by the complex cellular composition of the skin. The epidermis is the outermost layer composed of different strata made of keratinocytes (KC) from the most exposed surface to the least differentiated deeper area: stratum corneum, stratum granulosum, stratum spinosum, and stratum basale. Immune cells that ensure immunosurveillance such as Langerhans cells (LC) and specialized cells that produce melanin such as melanocytes are found in the epidermis. The dermis is the intermediate layer composed of several specialised immune cells such as plasmocytoid dendritic cells (pDC), dermal dendritic cells (dDC), macrophages (MØ), natural killer cells (NK), innate lymphoid cells (ILC), and T cells responsible of the immune response. In addition, blood and lymphatic vessels are present throughout the dermis. The hypodermis (not represented) is the innermost layer constituted mainly of adipose tissue.
Figure 3
Figure 3
Initiation of a primary cutaneous immune response. The skin is a primary immunological barrier to the external environment. The uppermost layer “corneal layer” is composed of dead keratinocytes that provide a physical barrier. However, the pathogens can access directly to the interior of the host through skin wounds and by outcompeting the normal flora (1). TLR-bearing cells (KCs and LCs) recognize pathogens and establish a highly coordinated immune response: antimicrobial production to neutralize the pathogen (2), inflammatory mediator secretion to alert the immune cells (3), activation of innate immune cells such as natural killer cells (NK) to induce cell lysis and/or phagocytosis such as macrophages to engulf pathogens (4), and maturation of dermal DCs that migrate into draining lymph nodes to prime T cell responses (adaptive immunity) (5).
Figure 4
Figure 4
Major actors of the adaptive immune response. The adaptive immune system mounts a stronger, antigen-specific immune response when the innate immune response fails to eliminate pathogens. The first phase consists of the activation of antigen-presenting cells such as DCs allowing their migration into lymph nodes where they prime naïve T cells. Activated T cells migrate back to the site of infection where they induce cell-mediated and humoral immunity causing mediator release by the immune cells present at the site of infection. The resulting cytokinic environment stimulates epidermal cells mainly KCs to release further mediators that activate and maintain the dermal immune response. Hence, a positive feedback loop forms. DCs: dendritic cells; KCs: keratinocytes; TH: T helper; MHC: major histocompatibility class; IFN: interferon; CD: cluster of differentiation; IL: interleukin; TNF: tumor necrosis factor.
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