Viral infections in atopic dermatitis Pathogenic aspects and clinical management

Wollenberg, Andreas; Wetzel, Stefanie; Burgdorf, Walter H. C.; Haas, Jürgen

doi:10.1016/j.jaci.2003.07.001

Cited by 266 publications

(278 citation statements)

References 58 publications

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“…One such example is the epidermotropic DNA virus Molluscum contagiosum expressing the viral CCR8 antagonist MC148 (19). Interestingly, Molluscum contagiosum infections show a markedly increased frequency in individuals with atopic dermatitis (20) suggesting that this DNA virus adapted to preferentially CCL1-CCR8-driven skin immune responses in atopic individuals.…”

Section: Discussionmentioning

confidence: 99%

CCL1-CCR8 Interactions: An Axis Mediating the Recruitment of T Cells and Langerhans-Type Dendritic Cells to Sites of Atopic Skin Inflammation

Gombert

Dieu-Nosjean

Winterberg

et al. 2005

The Journal of Immunology

184

142

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Atopic dermatitis represents a chronically relapsing skin disease with a steadily increasing prevalence of 10–20% in children. Skin-infiltrating T cells, dendritic cells (DC), and mast cells are thought to play a crucial role in its pathogenesis. We report that the expression of the CC chemokine CCL1 (I-309) is significantly and selectively up-regulated in atopic dermatitis in comparison to psoriasis, cutaneous lupus erythematosus, or normal skin. CCL1 serum levels of atopic dermatitis patients are significantly higher than levels in healthy individuals. DC, mast cells, and dermal endothelial cells are abundant sources of CCL1 during atopic skin inflammation and allergen challenge, and Staphylococcus aureus-derived products induce its production. In vitro, binding and cross-linking of IgE on mast cells resulted in a significant up-regulation of this inflammatory chemokine. Its specific receptor, CCR8, is expressed on a small subset of circulating T cells and is abundantly expressed on interstitial DC, Langerhans cells generated in vitro, and their monocytic precursors. Although DC maintain their CCR8+ status during maturation, brief activation of circulating T cells recruits CCR8 from intracytoplamic stores to the cell surface. Moreover, the inflammatory and atopy-associated chemokine CCL1 synergizes with the homeostatic chemokine CXCL12 (SDF-1α) resulting in the recruitment of T cell and Langerhans cell-like DC. Taken together, these findings suggest that the axis CCL1-CCR8 links adaptive and innate immune functions that play a role in the initiation and amplification of atopic skin inflammation.

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Section: Discussionmentioning

confidence: 99%

CCL1-CCR8 Interactions: An Axis Mediating the Recruitment of T Cells and Langerhans-Type Dendritic Cells to Sites of Atopic Skin Inflammation

Gombert

Dieu-Nosjean

Winterberg

et al. 2005

The Journal of Immunology

184

142

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“…Staphylococci frequently provoke an impetiginization of lesions in children leading to yellow, impetigo-like crusting. Patients with AD are at increased risk for fulminant herpes simplex virus infections (eczema herpeticum) 59 . The course of this complication may be severe with high fever and widespread eruptions.…”

Section: ) Complicationsmentioning

confidence: 99%

Atopic Dermatitis

2010

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“…3,4 Eczema herpeticum (ADEH) is a disseminated herpes simplex virus (HSV)-1 or -2 infection that occurs in a subset of patients with AD. 5,6 Left un-treated, ADEH may be fatal due to systemic viremia. 7 However, only a small subset of AD patients develop problems with recurrent viral infections, suggesting they may have an AMP phenotype distinct from most AD patients.…”

Section: Introductionmentioning

confidence: 99%