Role of vasculature in atopic dermatitis

Steinhoff, Martin; Steinhoff, Annekatrin; Homey, Bernhard; Luger, Thomas A.; Schneider, Stefan W.

doi:10.1016/j.jaci.2006.04.025

Cited by 44 publications

(29 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…30 AD lesions are characterized by activation of endothelial and vascular smooth muscle cells, which are ultimately involved in clinical symptoms of AD. 31 A secondary Raynaud-like phenomenon in AD has been observed with elevated ET-1 in infants with severe AD. 32 The circulating half-life of ET-1 is 2-3 minutes, and it is almost completely metabolized in the pulmonary capillaries by neutral endopeptidase.…”

Section: Discussionmentioning

confidence: 99%

Plasma endothelin-1 levels during exacerbation of atopic dermatitis

Цыбиков

Petrisheva²,

Кузник³

et al. 2015

allergy asthma proc

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Plasma endothelin-1 levels during exacerbation of atopic dermatitis

Цыбиков

Petrisheva²,

Кузник³

et al. 2015

allergy asthma proc

View full text Add to dashboard Cite

show abstract

“…65 AD skin inflammation develops as the result of a complex immune and inflammatory response driven by the release of proinflammatory cytokines and chemokines from multiple resident cell types including keratinocytes, Langerhans cells, monocyte/macrophages, and the cutaneous vascular system. [66][67][68] Hyperresponsive T H 2 cells with enhanced nuclear factor-kB activation also contribute to enhanced skin inflammation in animal models of AD. 69 During the past year, there was considerable interest in the identification of IL-31 in human AD skin, because it is a novel T H 2-derived cytokine known to cause severe pruritus and eczema in animal models.…”

Section: Admentioning

confidence: 99%

Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects

Sicherer

Leung

2007

Journal of Allergy and Clinical Immunology

View full text Add to dashboard Cite

This review highlights some of the research advances in anaphylaxis and hypersensitivity reactions to foods, drugs, and insects and in allergic skin disease that were reported primarily in the Journal in 2006. Advances in diagnosis include identification of food proteins to which IgE binding is associated with severe reactions; elucidation of diagnostic relationships of skin prick test wheal size with outcomes of egg, tree nut, and sesame allergy; evaluation of the diagnostic utility of atopy patch testing for food; and the observation that yellow jacket sting outcomes are influenced by species. Mechanistic observations include the following: heating of birch pollen-related foods disrupts IgE binding but not T-cell epitopes; a simple imbalance of T(H)1/T(H)2 response does not explain variations in clinical expression of peanut allergy; and elucidation of the role of dendritic cells in drug hypersensitivity. With regard to treatment, a rapidly disintegrating epinephrine tablet showed promise for sublingual treatment of anaphylaxis, RNA interference techniques showed promise in creating lower-allergenic foods, and anti-IL-5 showed promise for treatment of eosinophilic esophagitis. Progress in our understanding of the immunology and the etiology of skin barrier dysfunction in atopic dermatitis has also been made. These observations will likely contribute toward optimizing management of these common allergic disorders.

show abstract

“…For the inflammatory cells to infiltrate into the skin and cause inflammatory reaction, they must be recruited by the actions of some locally produced chemotactic factors present in the skin [44,45]. In addition, the inflammatory cells that infiltrate into the skin's affected sites must travel through blood vessels and need the assistance of microvascular endothelial cells by way of adhesion molecules [44,45].…”

Section: Role Of Chemokines and Adhesion Moleculesmentioning

confidence: 99%

“…In addition, the inflammatory cells that infiltrate into the skin's affected sites must travel through blood vessels and need the assistance of microvascular endothelial cells by way of adhesion molecules [44,45].…”

Section: Role Of Chemokines and Adhesion Moleculesmentioning

confidence: 99%

Atopic Dermatitis in 2008

Chan¹

2008

Current Directions in Autoimmunity

View full text Add to dashboard Cite

Atopic dermatitis (also termed atopic eczema and infantile eczema), a chronic, itchy, inflammatory skin disease that sets on at infancy or early childhood, is observed with increasing prevalence around the world, particularly in developed nations. Although sufficient evidences are not yet available to define it as a classical autoimmune disease, autoantigens have been identified. Investigations of atopic dermatitis in human patients and animal models suggest that this disease is initiated, maintained and perpetuated by the actions of cytokines, chemokines, T cells, antigen-presenting cells and other inflammatory cells; there is also evidence of skin barrier defect and angiogenesis. Recent identification of mutations of the epidermal barrier protein filaggrin (encoded by FLG), present in about 9% of people of European origin, with 70% of individuals homozygous or compound heterozygous for FLG null alleles developing atopic dermatitis, provides a strong link between a defect of the epidermal barrier that allows easy penetration of pathogen/allergen through the skin and a systemic hyperactive immune response to the penetrated pathogen/allergen. The newly introduced concept of 'intrinsic' and 'extrinsic' atopic dermatitis has fueled the debate among academic dermatologists as to how 'atopic' atopic dermatitis should be defined. Some recent advancements on the management options for atopic dermatitis are also discussed.

show abstract

Role of vasculature in atopic dermatitis

Cited by 44 publications

References 36 publications

Plasma endothelin-1 levels during exacerbation of atopic dermatitis

Plasma endothelin-1 levels during exacerbation of atopic dermatitis

Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects

Atopic Dermatitis in 2008

Contact Info

Product

Resources

About