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Immune Response Patterns in Non‐Communicable Inflammatory Skin

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Immune Response Patterns in Non‐Communicable Inflammatory Skin DOI: 10.1111/jdv.14673 JEADV REVIEW ARTICLE Immune response patterns in non-communicable inflammatory skin diseases K. Eyerich,1,* S. Eyerich2 1Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany 2ZAUM – Center of Allergy and Environment, Technical University and Helmholtz Center Munich, Munich, Germany *Correspondence: K. Eyerich. E-mail: [email protected] Abstract Non-communicable inflammatory skin diseases (ncISD) such as psoriasis or atopic eczema are a major cause of global disease burden. Due to their impact and complexity, ncISD represent a major challenge of modern medicine. Dermatol- ogy textbooks describe more than 100 different ncISD based on clinical phenotype and histological architecture. In the last decades, this historical description was complemented by increasing molecular knowledge – and this knowledge is now being translated into specific therapeutics. Combining the enormous advances made in lymphocyte immunology and molecular genetics with clinical and histological phenotyping reveals six immune response patterns of the skin – type I immune cells cause the lichenoid pattern characterized by immune-mediated cell death of keratinocytes; type II immune cells underlie the eczematous pattern with impaired epidermal barrier, infection and eosinophils as well as the bullous pattern with loss of epithelial integrity; Th17 cells and ILC3 mediate the psoriatic pattern characterized by acan- thosis, high metabolic activity and neutrophils; dysbalance of regulatory T cells causes either the fibrogenic pattern with rarefication of cells and dermal thickening or the granulomatous pattern defined by formation of granulomas. With more and more specific therapeutic agents approved, classifying ncISD also according to their immune response pattern will become highly relevant. This review defines the six immune response patterns of ncISD and highlights therapeutic strategies targeting key lymphocyte mediators. Received: 31 August 2017; Accepted: 19 October 2017 Conflicts of interest None declared. Funding sources None declared. An immunologic view at inflammatory skin recent advances made in design and approval of specific diseases immune-mediating therapeutics, a classification of ncISD Non-communicable inflammatory skin diseases (ncISD) are fre- according to their immune response patterns is required (Fig. 1, quent, affected individuals suffer from a devastating loss of qual- Tables 1 and 2). This review summarizes what is known about ity of life, and socio-economic costs are enormous. The complex immunology, histopathology and clinical phenotype for each of pathogenesis of ncISD is based on genetic predisposition and the immune response patterns. It further describes limitations of environmental influences that result in impaired epithelial func- the classification, early pathogenic events, and focuses on thera- tion and altered immunity. Historically, disease classification in peutic consequences and future developments. dermatology relies on precise clinical description in combination with histological description of microscopic tissue alterations Lichenoid pattern (pattern 1) and infiltrating immune cells. This classification is complex, and The major physiologic role of the lichenoid pattern is disposal of at times misleading. At the same time, insights into mechanisms keratinocytes that are potentially infected with intracellular how distinct lymphocyte subsets terminally orchestrate the microbes or are (pre-)carcinogenic due to DNA damages beyond inflammatory response and how these lymphocytes interact with repair. It is characterized by a cytotoxic immune response resident skin cells1 resulted in a translational revolution leading against keratinocytes of the basal layer (‘interface dermatitis’) to more and more specific therapeutics.2 To acknowledge these that is mediated by killer T cells (Tc1), Th1 cells, ILC1, NKT and JEADV 2018, 32, 692–703 © 2017 The Authors. Journal of the European Academy of Dermatology and Venereology published by John Wiley & Sons Ltd on behalf of European Academy of Dermatology and Venereology. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. Immune patterns in ncISD 693 Lichenoid IL-12 IFN-γ Th1/ TNF-α ILC1 PATTERN 1 PATTERN TBET Physiological role: cellular immunity a) Eczematous IL-4 Th2/ IL-4 ILC2 IL-5 IL-13 PATTERN 2 PATTERN b) Blistering GATA3 Physiological role: parasites/humoral immunity Precursor Th17/ IL-17 Psoriatic ILC3 IL-21 IL-1ß IL-22 IL-6 IL-23 RORc2 TGF-β IL-22 PATTERN 3 PATTERN TNF-α IL-6 Th22 TNF-α AHR Physiological role: a) Fibrogenic Barrier Homeostasis/ Wound Healing IL-10 iTreg IL-2 TGF-β b) Granulomatous TGF-β TTERN 4 PA FOXP3 Physiological role: limitation Figure 1 Lymphocyte subsets drive distinct response patterns in the skin. Distinct lymphocyte subgroups differentiate out of common na€ıve precursor cells under specific micro-environmental stimuli. Lymphocyte subsets are characterized by lineage-defining transcription factors as well as secreted cytokines. These cytokines elicit six distinct cutaneous response patterns. Shown are representative histologi- cal and clinical pictures of each response pattern. JEADV 2018, 32, 692–703 © 2017 The Authors. Journal of the European Academy of Dermatology and Venereology published by John Wiley & Sons Ltd on behalf of European Academy of Dermatology and Venereology. JEADV 694 2018, 32, 692 – 703 Table 1 Hallmarks of immune response patterns in ncISD 1 2a 2b 3 4a 4b Lichenoid Eczematous Bullous Psoriatic Fibrogenic Granulomatous © Clinical Polygonal papules, sharply Vesicles, papules, Bullae with surrounding Pustules, thick Skin thickening, epidermal Brownish/ yellowish 2017 The Authors. phenotype demarcated livid plaques, erythema, erosion, erythema, erosions, desquamation, sharply atrophy, telangiectasia, papules, without fine and shiny desquamation crusts, desquamation, crusts demarcated plaques papules without desquamation sebostasis desquamation Histological Interface dermatitis, Spongiosis, serum Acantholysis/ (micro)-abscess/ neutrophils, Presence of mucin/ amyloid, Presence of phenotype hypergranulosis, lymphocyte crusts, eosinophils, epidermolysis with regular acanthosis, dilated thickening of fibres, cellular Granulomas, normal or Journal of the European Academy of Dermatology and Venereology infiltration till deeper layers, oedema cellular infiltration capillaries rarefication, normal or atrophic epidermis cytoid bodies atrophic epidermis Patho-mechanism/ Apoptosis, necroptosis Downregulation of Direct lysis of antibody, Recruitment of neutrophils, Extracellular deposit of Granuloma formation molecular epithelial innate Opsonization Activation of epithelial innate peptides/ peptidoglycans/ phenotype immunity, immunity, mucins, growth factors Epithelial barrier Migration of epithelial cells, impairment, Downregulation of epithelial Eosinophil recruitment, differentiation, mast cell activation vascularization Major cytokines IFN-c IL-4, IL-5, IL-13, IL-31 IL-4, IL-5 IL-17A, IL-17F, IL-21, IL-22 TGF-b, IL-10, IL-10 TNF-a (non-Treg) on behalf of European Academy of Dermatology and Venereology. Biomarkers Skin: CXCL10, RIP-3, Fas/ Blood and skin: CCL17, Blood and skin: Specific Blood: HBD-2 Skin: Foxp3, COMP Skin: Adipophilin74 FasL, Caspase 3 CCL22 antibody levels Skin: IL-36, NOS2 published by John Wiley & Sons Ltd Eyerich and Eyerich JEADV Table 2 ncISD grouped into immune response patterns Immune patterns in ncISD 1 2a 2b 3 4a 4b 2018, Lichenoid Eczematous Bullous Psoriatic Fibrogenic Granulomatous 32, Alopecia areata Atopic eczema/ dermatitis Adult linear IgA bullous Acne vulgaris Amyloidosis (Ear amyloid; Actinic granuloma 692 dermatosis nodular) – Ashy dermatosis (Erythema Childhood granulomatous Brunsting-Perry cicatricial Acne keloidalis (Folliculitis Atrophoderma (Pierini-Pasini) Annular elastolytic giant cell 703 dyschronicum perstans) periorificial dermatitis† pemphigoid keloidalis nuchae) granuloma Benign lichenoid keratosis Chronic urticaria (cholinergic, Bullous pemphigoid (IgG, IgE Acne fulminans Eosinophilic fasciitis (Shulman) Cheilitis granulomatosis idiopathic, physical) type) (Miescher/ Melkersson- Rosenthal) Contact dermatitis†, allergic/ Chronic actinic dermatitis Chronic bullous dermatosis of Acne inversa (Hidradenitis Graft-vs.-host disease, Childhood granulomatous † fi † © photo-allergic/ photo-toxic/ childhood suppurativa) sclerodermatous periori cial dermatitis 2017 The Authors. irritant/ systemic Dermatomyositis Chronic superficial dermatitis/ Cicatricial pemphigoid Acrodermatitis continua Lichen amyloidosis Drug reaction, interstitial small plaque parapsoriasis† suppurativa (Hallopeau) granulomatous Drug eruption (lichenoid, Contact dermatitis†, allergic/ Dermatitis herpetiformis Acute febrile neutrophilic Hyalinosis cutis et mucosae Facial aseptic granuloma fixed) photo-allergic/ photo-toxic/ (Duhring) dermatosis (Sweet) (Urbach-Wiethe) Journal of the European Academy of Dermatology and Venereology irritant/ systemic Erythema multiforme DRESS syndrome Epidermolysis bullosa Acute generalized Keloid Foreign body granuloma acquisita exanthematous pustulosis Graft-vs.-host disease, Dyshidrotic eczema Lichen planus pemphigoides† Acute generalized pustular Lichen myxedematosus Granuloma annulare lichenoid bacterid (Andrews) Graft-vs.-host disease,
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