Phenotyping of epidermal dendritic cells allows the differentiation between extrinsic and intrinsic forms of atopic dermatitis

Oppel, Tilmann; Schuller, Erich; Günther, Sandra; Moderer, Martina; Haberstok, Jörg; Bieber, Thomas; Wollenberg, Andreas

doi:10.1046/j.1365-2133.2000.03887.x

Cited by 74 publications

(47 citation statements)

References 19 publications

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“…However, this upregulation of FcεRI surface expression cannot be observed when monocytes from patients with intrinsic AD are analyzed [21]. Lesional skin from intrinsic AD, although clinically similar to extrinsic AD, can be distinguished by a much lower FcεRI surface expression on epidermal DC [22].…”

Section: Fcεri Expression On Antigen-presenting Cells Is Associated Wmentioning

confidence: 96%

Immunoglobulin e-bearing antigen-presenting cells in atopic dermatitis

Novak

Bieber

Kraft

2004

Curr Allergy Asthma Rep

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Human antigen-presenting cells (APCs) bind monomeric immunoglobulin E (IgE) via the high-affinity IgE receptor, Fc epsilon RI. Surface expression of this trimeric structure is strongly associated with the atopic status of the donors, and maximal levels are observed on Langerhans cells (LC) and inflammatory dendritic epidermal cells (IDEC) in atopic dermatitis (AD). Although intracellular expression of the Fc epsilon RI alpha-chain is induced by interleukin-4 (IL-4), the upregulation of surface levels on dendritic cells (DC) from atopics is due to enhanced expression of the Fc epsilon RI gamma-chain and stabilization by binding of its ligand IgE. A characteristic function of Fc epsilon RI-bearing APCs is the specific uptake and processing of IgE-bound allergens, which is followed by T-cell stimulation. In AD, DC-mediated presentation of aeroallergens penetrating the epidermis is thought to induce an IgE-mediated, delayed-type hypersensitivity reaction. In addition, different Fc epsilon RI-bearing APC subsets in AD skin might regulate inflammatory processes through the production of Th1/Th2-polarizing signals, proinflammatory cytokines, chemokines, and factors that are involved in the induction of tolerance.

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Section: Fcεri Expression On Antigen-presenting Cells Is Associated Wmentioning

confidence: 96%

Immunoglobulin e-bearing antigen-presenting cells in atopic dermatitis

Novak

Bieber

Kraft

2004

Curr Allergy Asthma Rep

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“…This subgroup of AD, with the patients having normal IgE levels, has been labelled the intrinsic form of AD (IAD) [4]. In addition, epidermal dendritic cells of IAD patients have decreased levels of the high-affinity IgE receptor as compared with extrinsic AD (EAD) patients [5]. We have previously reported that both EAD patients (those having IgE sensitization) as well as IAD patients demonstrate predominantly T cells in the cellular infiltrate in eczematous skin lesions [6], suggesting a potential role of these cells in the pathogenesis of AD independent of IgE antibodies.…”

Section: Introductionmentioning

confidence: 99%

The Interleukin-13 Production by Peripheral Blood T Cells from Atopic Dermatitis Patients Does Not Require CD2 Costimulation

Simon¹,

Gunten²,

Borelli³

et al. 2003

Int Arch Allergy Immunol

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Background: Although allergic mechanisms appear to be important, the pathogenesis of both extrinsic and intrinsic forms of atopic dermatitis (AD) is unknown. Methods: We compared the cytokine production of peripheral blood mononuclear cells of extrinsic AD (EAD) and intrinsic AD (IAD) patients and normal control individuals after stimulation with anti-CD3 and/or anti-CD28 monoclonal antibodies (mAbs) in the presence or absence of anti-CD2-blocking mAb. The cytokine production was measured by immunoassays in supernatants of 24-hour cultures. Results: EAD patients showed a decreased capacity to synthesize interferon gamma and granulocyte-macrophage colony-stimulating factor upon anti-CD3 mAb stimulation as compared with IAD patients. Both EAD and IAD patients demonstrated an increased production of interleukin (IL)-5 and IL-13. As expected, interferon gamma, granulocyte-macrophage colony-stimulating factor, and IL-5 levels were reduced in the presence of anti-CD2-blocking mAbs. CD28 costimulation restored the release in cultures with anti-CD2 mAbs added, suggesting that CD2 and CD28 have redundant functions in T cell activation and subsequent cytokine production. Strikingly, the IL-13 production was not blocked by anti-CD2 mAbs and also not increased by agonistic anti-CD28 mAb, in particular within the EAD patient group. Conclusion: The signalling pathway initiated by the T cell receptor complex leading to increased IL-13 production in AD patients appears to be highly sensitive and is largely independent on CD2 costimulatory signals.

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“…Hence, patients may initially be considered having a nonallergic AEDS, but during the allergologic workup they may need to be reclassified as allergic AECS and vice versa. While nonallergic is clinically similar to allergic AEDS, the inflammatory microenvironment in these conditions seems to be different from classical allergic AEDS and can be clearly distinguished by phenotyping of epidermal dendritic cells (70).…”

Section: Nonallergic Aedsmentioning

confidence: 99%

Atopic eczema/dermatitis syndrome – a genetically complex disease. New advances in discovering the genetic contribution

Klüken¹,

Wienker

Bieber³

2003

Allergy

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Phenotyping of epidermal dendritic cells allows the differentiation between extrinsic and intrinsic forms of atopic dermatitis

Abstract: While IAD is clinically similar to EAD, the inflammatory microenvironment in this condition seems different from classical EAD and can be distinguished by phenotyping of epidermal DCs.

Cited by 74 publications

References 19 publications

Immunoglobulin e-bearing antigen-presenting cells in atopic dermatitis

Immunoglobulin e-bearing antigen-presenting cells in atopic dermatitis

The Interleukin-13 Production by Peripheral Blood T Cells from Atopic Dermatitis Patients Does Not Require CD2 Costimulation

Atopic eczema/dermatitis syndrome – a genetically complex disease. New advances in discovering the genetic contribution

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