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• W2015784582 abstract "Atopic dermatitis (AD) is a common pruritic and chronically relapsing inflammatory skin disease. The pathophysiology of AD includes disturbed skin barrier functions, frequent allergic responses against allergens, defects in the antimicrobial immune defense, and a genetic predisposition. In this review we summarize advances in our understanding of the complex interdependent network of members of the rapidly growing protein superfamilies of cytokines and chemokines that lead to the development of AD. Atopic dermatitis (AD) is a common pruritic and chronically relapsing inflammatory skin disease. The pathophysiology of AD includes disturbed skin barrier functions, frequent allergic responses against allergens, defects in the antimicrobial immune defense, and a genetic predisposition. In this review we summarize advances in our understanding of the complex interdependent network of members of the rapidly growing protein superfamilies of cytokines and chemokines that lead to the development of AD. Atopic dermatitis (AD) is a common pruritic and chronically relapsing inflammatory skin disease with a steadily increasing prevalence. Endogenous, as well as exogenous, factors play a role in the manifestation of this disease, which has a serious effect on patients, their families, and socioeconomic aspects of life. The pathophysiology of AD includes a disturbed skin barrier function (for review, see article by Cork et al1Cork M.J. Robinson D.A. Vasilopoulos Y. Ferguson A. Moustafa M. MacGowan A. et al.New perspectives on epidermal barrier dysfunction in atopic dermatitis: gene–environment interactions.J Allergy Clin Immunol. 2006; 118: 3-21Abstract Full Text Full Text PDF PubMed Scopus (416) Google Scholar in this issue of the Journal), frequent allergic responses against allergens, defects in the antimicrobial immune defense, and a genetic predisposition. Recent studies provide insights into the underlying immunologic mechanisms, suggesting an amplification cycle of atopic skin inflammation. In this review we summarize advances in our understanding of the complex interdependent network of members of the rapidly growing protein superfamilies of cytokines and chemokines that lead to the development of AD. Clinical observations in AD combined with the results of recent scientific studies suggest an amplification cycle of atopic skin inflammation (Fig 1). This cycle might start with pruritus, representing a prominent symptom of AD.2Steinhoff M, Bienenstock J, Schmelz M, Maurer M, Wei E, Biro T. Neurophysiological, neuroimmunological and neuroendocrine basis of pruritus. J Invest Dermatol. In press 2006.Google Scholar Patients scratch and induce mechanical injury, resulting in proinflammatory cytokine and chemokine production. Subsequently, chemokines, in concert with an array of adhesion molecules, direct the recruitment of pathogenic leukocytes to the skin.3Homey B. Alenius H. Muller A. Soto H. Bowman E.P. Yuan W. et al.CCL27-CCR10 interactions regulate T cell-mediated skin inflammation.Nat Med. 2002; 8: 157-165Crossref PubMed Scopus (639) Google Scholar, 4Leung D.Y. Bieber T. Atopic dermatitis.Lancet. 2003; 361: 151-160Abstract Full Text Full Text PDF PubMed Scopus (1163) Google Scholar, 5Reiss Y. Proudfoot A.E. Power C.A. Campbell J.J. Butcher E.C. CC chemokine receptor (CCR)4 and the CCR10 ligand cutaneous T cell-attracting chemokine (CTACK) in lymphocyte trafficking to inflamed skin.J Exp Med. 2001; 194: 1541-1547Crossref PubMed Scopus (440) Google Scholar, 6Campbell J.J. Butcher E.C. Chemokines in tissue-specific and microenvironment-specific lymphocyte homing.Curr Opin Immunol. 2000; 12: 336-341Crossref PubMed Scopus (554) Google Scholar Within the skin, distinct leukocyte subsets can become activated through different pathways: (1) epithelial cell–derived cytokines (eg, thymic stromal lymphopoietin [TSLP]) instruct dendritic cells (DCs) to induce TH2 cell differentiation7Gilliet M. Soumelis V. Watanabe N. Hanabuchi S. Antonenko S. de Waal-Malefyt R. et al.Human dendritic cells activated by TSLP and CD40L induce proallergic cytotoxic T cells.J Exp Med. 2003; 197: 1059-1063Crossref PubMed Scopus (121) Google Scholar, 8Li M. Messaddeq N. Teletin M. Pasquali J.L. Metzger D. Chambon P. Retinoid X receptor ablation in adult mouse keratinocytes generates an atopic dermatitis triggered by thymic stromal lymphopoietin.Proc Natl Acad Sci U S A. 2005; 102: 14795-14800Crossref PubMed Scopus (170) Google Scholar, 9Liu Y.J. Thymic stromal lymphopoietin: master switch for allergic inflammation.J Exp Med. 2006; 203: 269-273Crossref PubMed Scopus (455) Google Scholar, 10Yoo J. Omori M. Gyarmati D. Zhou B. Aye T. Brewer A. et al.Spontaneous atopic dermatitis in mice expressing an inducible thymic stromal lymphopoietin transgene specifically in the skin.J Exp Med. 2005; 202: 541-549Crossref PubMed Scopus (464) Google Scholar, 11Soumelis V. Reche P.A. Kanzler H. Yuan W. Edward G. Homey B. et al.Human epithelial cells trigger dendritic cell mediated allergic inflammation by producing TSLP.Nat Immunol. 2002; 3: 673-680Crossref PubMed Scopus (338) Google Scholar; (2) memory T cells encounter their specific antigen-allergen (eg, Der p 2 from house dust mites) or bacterial superantigens (eg, staphylococcal enterotoxins)4Leung D.Y. Bieber T. Atopic dermatitis.Lancet. 2003; 361: 151-160Abstract Full Text Full Text PDF PubMed Scopus (1163) Google Scholar; (3) DCs bind antigen–specific IgE complexes, capture antigen, and show enhanced antigen presentation capabilities4Leung D.Y. Bieber T. Atopic dermatitis.Lancet. 2003; 361: 151-160Abstract Full Text Full Text PDF PubMed Scopus (1163) Google Scholar; (4) antigen–specific IgE complexes induce Fcε receptor aggregation and activate mast cells4Leung D.Y. Bieber T. Atopic dermatitis.Lancet. 2003; 361: 151-160Abstract Full Text Full Text PDF PubMed Scopus (1163) Google Scholar; and (5) viruses, fungi, and bacteria take advantage of a reduced level of antimicrobial peptides present in AD skin, colonize inflamed skin, and release proinflammatory products, resulting in the modulation and amplification of leukocyte activation.12Nomura I. Gao B. Boguniewicz M. Darst M.A. Travers J.B. Leung D.Y. Distinct patterns of gene expression in the skin lesions of atopic dermatitis and psoriasis: a gene microarray analysis.J Allergy Clin Immunol. 2003; 112: 1195-1202Abstract Full Text Full Text PDF PubMed Scopus (274) Google Scholar, 13Ong P.Y. Ohtake T. Brandt C. Strickland I. Boguniewicz M. Ganz T. et al.Endogenous antimicrobial peptides and skin infections in atopic dermatitis.N Engl J Med. 2002; 347: 1151-1160Crossref PubMed Scopus (1611) Google Scholar As a common feature, leukocyte activation results in the release of inflammatory mediators, including effector cytokines (IL-31) and proteases (tryptase), which, together with stress-induced neuropeptides, perpetuate pruritic signals.2Steinhoff M, Bienenstock J, Schmelz M, Maurer M, Wei E, Biro T. Neurophysiological, neuroimmunological and neuroendocrine basis of pruritus. J Invest Dermatol. In press 2006.Google Scholar, 14Dillon S.R. Sprecher C. Hammond A. Bilsborough J. Rosenfeld-Franklin M. Presnell S.R. et al.Interleukin 31, a cytokine produced by activated T cells, induces dermatitis in mice.Nat Immunol. 2004; 5: 752-760Crossref PubMed Scopus (721) Google Scholar, 15Schmelz M. Itch—mediators and mechanisms.J Dermatol Sci. 2002; 28: 91-96Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar, 16Steinhoff M. Neisius U. Ikoma A. Fartasch M. Heyer G. Skov P.S. et al.Proteinase-activated receptor-2 mediates itch: a novel pathway for pruritus in human skin.J Neurosci. 2003; 23: 6176-6180PubMed Google Scholar Taken together, these amplifying processes sustain inflammatory responses within the skin and lead to the development of an AD phenotype. Little is known about the very early events initiating atopic skin inflammation. However, the production of primary proinflammatory cytokines after mechanical trauma and skin barrier disruption is a well-accepted scenario. Clinically, patients with AD show significantly lower itch thresholds and do not have skin lesions unless they scratch. Furthermore, experimental studies in mice support that the itch-scratch cycle is important for the development of dermatitis.17Mihara K. Kuratani K. Matsui T. Nakamura M. Yokota K. Vital role of the itch-scratch response in development of spontaneous dermatitis in NC/Nga mice.Br J Dermatol. 2004; 151: 335-345Crossref PubMed Scopus (74) Google Scholar Numerous studies showed that mechanical trauma and skin barrier disruption after tape stripping of the skin results in the rapid and marked upregulation of IL-1α, IL-1β, TNF-α, and GM-CSF.18Wood L.C. Jackson S.M. Elias P.M. Grunfeld C. Feingold K.R. Cutaneous barrier perturbation stimulates cytokine production in the epidermis of mice.J Clin Invest. 1992; 90: 482-487Crossref PubMed Scopus (407) Google Scholar, 19Wood L.C. Elias P.M. Calhoun C. Tsai J.C. Grunfeld C. Feingold K.R. Barrier disruption stimulates interleukin-1 alpha expression and release from a pre-formed pool in murine epidermis.J Invest Dermatol. 1996; 106: 397-403Crossref PubMed Scopus (243) Google Scholar These primary proinflammatory cytokines in turn induce the production of chemoattractants and adhesion molecules (eg, intercellular adhesion molecule 1), supporting the recruitment, proliferation, and survival of leukocytes at cutaneous sites. Next to mechanical trauma, the staphylococcal product peptidoglycan and histamine have been suggested to contribute to the increased expression of GM-CSF in keratinocytes within the lesional skin of patients with AD.20Matsubara M. Harada D. Manabe H. Hasegawa K. Staphylococcus aureus peptidoglycan stimulates granulocyte macrophage colony-stimulating factor production from human epidermal keratinocytes via mitogen-activated protein kinases.FEBS Lett. 2004; 566: 195-200Abstract Full Text Full Text PDF PubMed Scopus (31) Google Scholar, 21Kanda N. Watanabe S. Histamine enhances the production of granulocyte-macrophage colony-stimulating factor via protein kinase C alpha and extracellular signal-regulated kinase in human keratinocytes.J Invest Dermatol. 2004; 122: 863-872Crossref PubMed Scopus (41) Google Scholar Hence GM-CSF is regulated under the control of innate and adaptive immune pathways and might support the survival and retention of DC subsets at sites of atopic skin inflammation. Recently, a member of the rapidly expanding IL-1 superfamily, IL-18, has been shown to participate in the development of a relapsing dermatitis with mastocytosis, TH2 cytokine accumulation, and systemic increase of IgE and histamine levels.22Konishi H. Tsutsui H. Murakami T. Yumikura-Futatsugi S. Yamanaka K. Tanaka M. et al.IL-18 contributes to the spontaneous development of atopic dermatitis-like inflammatory skin lesion independently of IgE/stat6 under specific pathogen-free conditions.Proc Natl Acad Sci U S A. 2002; 99: 11340-11345Crossref PubMed Scopus (212) Google Scholar Various cell types, including macrophages and keratinocytes, store IL-18 as a biologically inactive precursor. Caspase-1 or caspase-like enzymes cleave pro-IL-18 and release the active form after stimulation by danger signals. Simultaneous skin-specific expression of IL-18 and caspase-1 leads to this atopy-like dermatitis.22Konishi H. Tsutsui H. Murakami T. Yumikura-Futatsugi S. Yamanaka K. Tanaka M. et al.IL-18 contributes to the spontaneous development of atopic dermatitis-like inflammatory skin lesion independently of IgE/stat6 under specific pathogen-free conditions.Proc Natl Acad Sci U S A. 2002; 99: 11340-11345Crossref PubMed Scopus (212) Google Scholar Interestingly, the dermatitis phenotype is independent of signal transducer and activator of transcription 6–signaling pathways but critically dependent on the presence of active IL-18.22Konishi H. Tsutsui H. Murakami T. Yumikura-Futatsugi S. Yamanaka K. Tanaka M. et al.IL-18 contributes to the spontaneous development of atopic dermatitis-like inflammatory skin lesion independently of IgE/stat6 under specific pathogen-free conditions.Proc Natl Acad Sci U S A. 2002; 99: 11340-11345Crossref PubMed Scopus (212) Google Scholar Therefore Konishi et al22Konishi H. Tsutsui H. Murakami T. Yumikura-Futatsugi S. Yamanaka K. Tanaka M. et al.IL-18 contributes to the spontaneous development of atopic dermatitis-like inflammatory skin lesion independently of IgE/stat6 under specific pathogen-free conditions.Proc Natl Acad Sci U S A. 2002; 99: 11340-11345Crossref PubMed Scopus (212) Google Scholar suggest that IL-18 induces IgE-independent allergic disorders and mediates an innate-type of allergic response. In contrast to these findings, Higa et al23Higa S. Kotani M. Matsumoto M. Fujita A. Hirano T. Suemura M. et al.Administration of anti-interleukin 18 antibody fails to inhibit development of dermatitis in atopic dermatitis-model mice NC/Nga.Br J Dermatol. 2003; 149: 39-45Crossref PubMed Scopus (8) Google Scholar could not demonstrate a role for IL-18 in the development of AD-like skin lesions in NC/Nga mice. Although IL-18 serum levels were significantly increased before and during the development in NC/Nga mice, administration of a neutralizing antibody failed to inhibit the onset and development of dermatitis and IgE level increase. The treatment, rather, tended to lead to an exacerbation of dermatitis and scratching behavior.23Higa S. Kotani M. Matsumoto M. Fujita A. Hirano T. Suemura M. et al.Administration of anti-interleukin 18 antibody fails to inhibit development of dermatitis in atopic dermatitis-model mice NC/Nga.Br J Dermatol. 2003; 149: 39-45Crossref PubMed Scopus (8) Google Scholar Keeping in mind that genetic approaches, intervention studies with neutralizing antibodies, and murine models for human diseases have their own limitations, the findings of a recent study by Novak et al24Novak N. Kruse S. Potreck J. Maintz L. Jenneck C. Weidinger S. et al.Single nucleotide polymorphisms of the IL18 gene are associated with atopic eczema.J Allergy Clin Immunol. 2005; 115: 828-833Abstract Full Text Full Text PDF PubMed Scopus (100) Google Scholar support a role for IL-18 in the pathogenesis of AD. Single nucleotide polymorphisms in exon 1 and the promoter region of the IL18 gene were significantly associated with an AD phenotype. These associations were independent of the concomitant manifestation of allergic rhinitis or asthma. Furthermore, the amount of IL-18 in the supernatants of PBMCs of patients with AD stimulated with staphylococcal enterotoxin B was significantly higher than that in healthy control subjects. In parallel, the amount of active IL-18 in the sera of patients with AD was enhanced at the exacerbation of their disease. These observations suggest that single nucleotide polymorphisms in the IL18 gene might be involved in the development of AD by contributing to a functional dysregulation of the IL-18 production in vivo.24Novak N. Kruse S. Potreck J. Maintz L. Jenneck C. Weidinger S. et al.Single nucleotide polymorphisms of the IL18 gene are associated with atopic eczema.J Allergy Clin Immunol. 2005; 115: 828-833Abstract Full Text Full Text PDF PubMed Scopus (100) Google Scholar Taken together, a set of primary proinflammatory cytokines might be induced through mechanical trauma and skin barrier disruption, initiating inflammation in atopic individuals. Furthermore, staphylococcal and mast cell products might sustain the release of these mediators and support the cycle of inflammation. Next to adhesion molecules, a new family of small cytokine-like proteins, the chemokines, has attracted significant interest with regard to understanding the mechanisms of leukocyte trafficking.25Butcher E.C. Picker L.J. 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Chemokines: a new classification system and their role in immunity.Immunity. 2000; 12: 121-127Abstract Full Text Full Text PDF PubMed Scopus (3232) Google Scholar To date, 45 human chemokine ligands have been identified, and this superfamily is thought to be among the first functional protein families completely characterized at the molecular level. On the basis of the arrangement of the amino terminal cysteine residues, chemokines can be divided into 4 subclasses: (1) CXC chemokines (termed CXC ligands [CXCLs]), (2) CC chemokines (CCL), (3) C chemokines (XCL), and (4) CX3C chemokine (CX3CL).27Rossi D. Zlotnik A. The biology of chemokines and their receptors.Annu Rev Immunol. 2000; 18: 217-242Crossref PubMed Scopus (2083) Google Scholar Chemokines bind pertussis toxin–sensitive, 7-transmembrane–spanning, G protein–coupled receptors. To date, 10 CC chemokine, 7 CXC chemokine, 1 CX3C, and 1 XCR receptors have been characterized.28Zlotnik A. Yoshie O. 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Picker L.J. Lymphocyte homing and homeostasis.Science. 1996; 272: 60-66Crossref PubMed Scopus (2493) Google Scholar From perivascular spaces, matrix-bound sustained chemokine gradients direct skin-infiltrating leukocyte subsets to subepidermal or intraepidermal locations. Several homeostatic and inflammatory chemokines, including CCL1, CCL2, CCL3, CCL4, CCL5, CCL11, CCL13, CCL18, CCL20, CCL22, CCL26 and CCL27, have been shown to be associated with an AD phenotype and might support leukocyte recruitment (Table I).3Homey B. Alenius H. Muller A. Soto H. Bowman E.P. Yuan W. et al.CCL27-CCR10 interactions regulate T cell-mediated skin inflammation.Nat Med. 2002; 8: 157-165Crossref PubMed Scopus (639) Google Scholar, 30Gombert M. Dieu-Nosjean M.C. Winterberg F. Bünemann E. Kubitza R.C. 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Expression of fractalkine and its receptor, CX3CR1, in atopic dermatitis: possible contribution to skin inflammation.J Allergy Clin Immunol. 2004; 113: 940-948Abstract Full Text Full Text PDF PubMed Scopus (72) Google Scholar Moreover, serum levels of CCL11, CCL17, CCL22, CCL26, CCL27, and CX3CL1 directly correlated with disease activity, suggesting an important role in the pathogenesis of AD (Table I).Table IAD-associated chemokines and their receptorsChemokine ligandCell of originIncreased serum/plasma levelsCorresponding receptor(s)Target cell(s)ReferencesCCL1/I-309Keratinocytes, endothelial cells, mast cellsYesCCR8T cells, LC precursors30Gombert M. Dieu-Nosjean M.C. Winterberg F. Bünemann E. Kubitza R.C. Da Cunha L. et al.CCL1-CCR8 interactions: an axis mediating the recruitment of T cells and Langerhans-type dendritic cells to sites of atopic skin inflammation.J Immunol. 2005; 174: 5082-5091PubMed Google ScholarCCL2/MCP-1Keratinocytes, leukocytesYesCCR2Monocytes, DC precursors31Kaburagi Y. Shimada Y. Nagaoka T. Hasegawa M. Takehara K. Sato S. Enhanced production of CC-chemokines (RANTES, MCP-1, MIP-1alpha, MIP-1beta, and eotaxin) in patients with atopic dermatitis.Arch Dermatol Res. 2001; 293: 350-355Crossref PubMed Scopus (111) Google ScholarCCL3/MIP-1αLeukocytesYesCCR1, CCR5Monocytes, T cells31Kaburagi Y. Shimada Y. Nagaoka T. Hasegawa M. Takehara K. Sato S. Enhanced production of CC-chemokines (RANTES, MCP-1, MIP-1alpha, MIP-1beta, and eotaxin) in patients with atopic dermatitis.Arch Dermatol Res. 2001; 293: 350-355Crossref PubMed Scopus (111) Google ScholarCCL4/MIP-1βLeukocytesYesCCR5Monocytes, T cells31Kaburagi Y. Shimada Y. Nagaoka T. Hasegawa M. Takehara K. Sato S. Enhanced production of CC-chemokines (RANTES, MCP-1, MIP-1alpha, MIP-1beta, and eotaxin) in patients with atopic dermatitis.Arch Dermatol Res. 2001; 293: 350-355Crossref PubMed Scopus (111) Google ScholarCCL5/RANTESKeratinocytes, leukocytesYesCCR1, CCR3, CCR5Eosinophils, T cells, fibroblasts31Kaburagi Y. Shimada Y. Nagaoka T. Hasegawa M. Takehara K. Sato S. Enhanced production of CC-chemokines (RANTES, MCP-1, MIP-1alpha, MIP-1beta, and eotaxin) in patients with atopic dermatitis.Arch Dermatol Res. 2001; 293: 350-355Crossref PubMed Scopus (111) Google Scholar, 32Gluck J. Rogala B. Chemokine RANTES in atopic dermatitis.Arch Immunol Ther Exp (Warsz). 1999; 47: 367-372PubMed Google Scholar, 33Niwa Y. Elevated RANTES levels in plasma or skin and decreased plasma IL-10 levels in subsets of patients with severe atopic dermatitis.Arch Dermatol. 2000; 136: 125-126Crossref PubMed Scopus (33) Google Scholar, 34Park C.W. Lee B.H. Han H.J. Lee C.H. Ahn H.K. 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