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Book:
Clinical and Basic Immunodermatology
Author:
Anthony A Gaspari / Stephen K Tyring and Daniel H Kaplan
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Springer International Publishing, Cham
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2017
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Springer International Publishing Switzerland 2017

Anthony A. Gaspari , Stephen K. Tyring and Daniel H. Kaplan (eds.) Clinical and Basic Immunodermatology 10.1007/978-3-319-29785-9_1

1. Innate and Adaptive Components of the Cutaneous Immune Barrier: The Central Role of Dendritic Cells

Georg Stingl 1

(1)

Department of Dermatology, Medical University of Vienna, Vienna, Austria

(2)

Division of Immunology, Allergy and Infectious Diseases, Department of Dermatology, Medical University of Vienna, Vienna, Austria

Georg Stingl (Corresponding author)

Email:

Marie-Charlotte Brggen

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Mariana Vzquez-Strauss

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Abstract

Immune responses initiated in the skin can be extremely powerful at both a local and systemic level. One of the milestones in elucidating the mechanisms underlying this phenomenon was the discovery of the T cell response-inducing function of Langerhans cells (LC). In the meantime, we know that the family of dendritic antigen-presenting cells in the skin is much bigger and, in addition to LC, includes dermal dendritic cells (DDC), CD141 + DC, CD14 + DC, inflammatory DC and plasmacytoid DC. Depending on the cellular and molecular milieu, these cells can function as either sensitizing or tolerizing elements. Signals transmitted from (innate) receptors recognizing damage- or pathogen-associated patterns are involved in directing these different functions in DC. Toll-like pathogen recognition receptors (TLR) have been particularly well investigated in this regard. The distinct distribution of TLR on LC and other DC subsets allows the immune system to elegantly orchestrate the regulatory and pro-inflammatory functions of these cells. Intriguingly, TLR signaling in DC/LC not only allows to initiate adaptive immune responses, but also directly induces innate effector functions. This is demonstrated by our findings on the mechanisms underlying basal cell carcinoma (BCC) regression upon treatment with the pharmacological TLR7 agonist imiquimod. We observed that in imiquimod-treated BCC, plasmacytoid DC directly kill tumor cells via the apoptosis-inducing molecule TRAIL. Melanoma cells can also become TRAIL-susceptible, but the magnitude of this phenomenon varies from patient to patient. Our recent findings show that TRAIL susceptibility of melanoma cell lines can be increased upon exposure to the anti-inflammatory compound diclofenac.

Taken together, we begin to understand the exact position of LC and DC in the highly complex circuits of the immune system in the skin and how these cells could be manipulated for therapeutic purposes.

Keywords

Dendritic cells Antigen-presenting cell APC BCC Basal cell carcinoma Contact hypersensitivity Dermal dendritic cell DC DDC Lipopolysaccharides Lipotechoic acid Adaptive immunity TLR-transmitted

Abbreviations

APC

Antigen-presenting cell

BCC

Basal cell carcinoma

CHS

Contact hypersensitivity

Dendritic cell

DDC

Dermal dendritic cell

dsRNA

Double-strain RNA

Langerhans cell

LPS

Lipopolysaccharides

LTA

Lipotechoic acid

MHC

Majory histocompatibility complex

PAMP

Pathogen-associated molecular pattern

pDC

Plasmacytoid dendritic cell

PRR

Pattern recognition receptor

Staphylococcus

ssRNA

Single-stranded RNA

TLR

Toll-like receptor

TRAIL

Tumor necrosis factor related apoptosis inducing ligand

Ultraviolet

poly I:C

Polyinosinic:polycytidylic acid

Introduction

One of the first documented examples revealing the potency of immune responses initiated in the skin is the successful smallpox vaccination by Edward Jenner []. In this heroic experiment performed on the son of his gardener, Jenner introduced scraping material obtained from an infectious cowpox pustule (of a dairymaid) into the skin. A few weeks later, upon re-inoculation with material from a fresh smallpox lesion, the boy was protected from the disease.

It took quite a while until it was realized that immunization via the skin can result in a stronger, longer lasting immune response than immunization via other routes. This is impressively illustrated by the induction of cancer immunity, which succeeded following the repeated intracutaneous, but not extracutaneous application of cancer (murine sarcoma) homogenates []. During the following decades, considerable efforts were made to unravel the mechanisms underlying this phenomenon.

The enigma seemed resolved when it was discovered that epidermal dendritic cells (namely Langerhans cells (LC)) can evoke very robust proliferative responses in naive and sensitized T cells [].

Fig. 1.1

LC and DC populations in human skin. ( a ) LC and DC residing in human skin in the steady state and ( b ) infiltrating the skin during inflammation. The main suface markers and pattern recognition receptors of the respective subpopulations are depicted

From a conceptual viewpoint, it makes perfect sense to assume that danger signals not reaching beyond the epidermis, i.e. the site of LC, will not mobilize all the armed forces the immune system is capable of activating. On the other hand, virulent microorganisms that breach the dermo-epidermal junction and thereby can reach DDC should trigger a massive host defense response that can successfully eliminate the pathogen. From this perspective, one would expect that LC mainly act as regulatory antigen-presenting cells (APC) inducing a state of antigen-specific non-responsiveness. Following this reasoning, DDC should remain inert under homoeostatic conditions and mature into potent sensitizing DC upon receiving appropriate activation signals. The black and white picture of the roles of LC vs. DC is probably not tenable under all circumstances. As an example, in response to an overwhelming microbial insult, LC can engage themselves in the promotion of a T effector cell response [].

In an inflammatory setting, skin-resident LC, DDC and CD141+ DC undergo phenotypic and functional changes. In addition, various other types of DC are entering the stage (cf. Fig). Their involvement in these diseases will be discussed in the respective chapters of this book.

Toll-Like Receptors: Bridging Innate and Adaptive Immunity

Pattern Recognition Receptors: Sensing the Danger

Until quite recently, it was essentially unknown by which mechanisms danger signals (such as immunogenic haptens and microorganisms) trigger the activation and maturation of LC and other DC in the skin and ultimately initiate an adaptive immune response. A series of discoveries (for review, cf. [). TLR can be broadly divided into two groups (extra- vs. intracellular). Extracellular TLR (TLR1, 2, 4, 5, 6) essentially recognize bacterial and fungal products. Briefly, TLR2 combined with TLR1 or TLR6 mostly recognizes motifs of gram-positive bacteria (e.g. lipoproteins, lipotechoic acid (LTA)), while TLR4 senses gram-negative bacteria-associated lipopolysaccharides (LPS). Bacterial flagellin is recognized by TLR5. The intracellular receptors TLR3 and TLR7-9 recognize mostly virus-derived nucleic acids, i.e. double-stranded RNA (dsRNA; TLR3), single-stranded RNA (ssRNA) (TLR7-8) and CpG oligodeoxynucleotides (TLR9).

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