Evaluation of the staphylococcal exotoxins and their specific IgE in childhood atopic dermatitis☆☆☆

Nomura, Ichiro; Tanaka, Kazuaki; Tomita, Hisashi; Katsunuma, Toshio; Ohya, Yukihiro; Ikeda, Norikazu; Takeda, Tae; Saito, Hirohisa; Akasawa, Akira

doi:10.1016/s0091-6749(99)70390-8

Cited by 134 publications

(110 citation statements)

References 14 publications

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“…Several studies also indicate that severe AD is associated with skin colonization of SEB-producing strains of S. aureus (5,23,24). To better understand the role of SEB in AD, we took advantage of the murine model of AD and investigated the effects of cutaneous SEB exposure in the modulation of allergen-induced skin inflammation.…”

Section: Discussionmentioning

confidence: 99%

Topical Superantigen Exposure Induces Epidermal Accumulation of CD8+ T Cells, a Mixed Th1/Th2-Type Dermatitis and Vigorous Production of IgE Antibodies in the Murine Model of Atopic Dermatitis

Savinko

Lauerma²,

Lehtimäki

et al. 2005

The Journal of Immunology

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Patients with atopic dermatitis (AD) have repeated cutaneous exposure to both environmental allergens and superantigen-producing strains of Staphylococcus aureus. We used a murine model of AD to investigate the role of staphylococcal enterotoxin B (SEB) in the modulation of allergen-induced skin inflammation. Mice were topically exposed to SEB, OVA, a combination of OVA and SEB (OVA/SEB), or PBS. Topical SEB and OVA/SEB exposure induced epidermal accumulation of CD8+ T cells and TCRVβ8+ cells in contrast to OVA application, which induced a mainly dermal infiltration of CD4+ cells. SEB and OVA/SEB exposure elicited a mixed Th1/Th2-associated cytokine and chemokine expression profile within the skin. Restimulation of lymph node cells from OVA- and OVA/SEB-exposed mice with OVA elicited strong production of IL-13 protein, whereas substantial amounts of IFN-γ protein were detected after SEB stimulation of cells derived from SEB- or OVA/SEB-exposed mice. Topical SEB treatment elicited vigorous production of SEB-specific IgE and IgG2a Abs and significantly increased the production of OVA-specific IgE and IgG2a Abs. The present study shows that topical exposure to SEB provokes epidermal accumulation of CD8+ T cells, a mixed Th2/Th1 type dermatitis and vigorous production of specific IgE and IgG2a Abs, which can be related to the chronic phase of atopic skin inflammation.

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Section: Discussionmentioning

confidence: 99%

Topical Superantigen Exposure Induces Epidermal Accumulation of CD8+ T Cells, a Mixed Th1/Th2-Type Dermatitis and Vigorous Production of IgE Antibodies in the Murine Model of Atopic Dermatitis

Savinko

Lauerma²,

Lehtimäki

et al. 2005

The Journal of Immunology

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“…To exclude the possibility that the dermatitis was associated with fur mites 30 or bacterial infection, 31,32 causes of dermatitis that have been previously reported, we performed parasitologic and bacteriologic examinations. No fur mites were found in the hair of mice with AD-like lesions or control mice.…”

Section: Microbiological Examinationmentioning

confidence: 99%

Murine model of atopic dermatitis associated with food hypersensitivity

Kleiner²,

Huang³

et al. 2001

Journal of Allergy and Clinical Immunology

111

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Background: Atopic dermatitis (AD) is an eczematous skin eruption that generally begins in early infancy and affects up to 12% of the population. The cause of this disorder is not fully understood, although it is frequently the first sign of atopic disease and is characterized by an elevated serum IgE level, eosinophilia, and histologic tissue changes characterized early by spongiosis and a CD4 + T H 2 cellular infiltrate. Hypersensitivity to foods has been implicated as one causative factor in up to 40% of children with moderate-to-severe AD. Objective: The purpose of this study was to establish a murine model of food-induced AD. Methods: Female C3H/HeJ mice were sensitized orally to cow's milk or peanut with a cholera toxin adjuvant and then subjected to low-grade allergen exposure. Histologic examination of skin lesions, allergen-specific serum Ig levels, and allergen-induced T-cell proliferation and cytokine production were examined. Atopic dermatitis (AD) is a form of eczema that generally begins in early infancy and is characterized by extreme pruritus, chronically relapsing course, and distinctive distribution. AD is often the first sign seen in a child who is prone to atopic disease, with 50% of all AD developing in the first year of life and 80% developing by 5 years of age. 1 In chronic skin lesions the epidermis has moderate-to-marked hyperplasia, with elongation of the rete ridges and prominent hyperkeratosis. Spongiosis is variable, and the numbers of mast cells and Langerhans cells are significantly increased. 2,3 Eosinophils are sparse, although eosinophil products (major basic protein) are prominent. 4 Although the pathogenic role of allergy in AD has been debated for over a century, clinical studies over the past 2 decades have supported the pathogenic role of food allergy in a subset of patients with AD. 5-7 A recent study found that approximately 40% of children with moderate-to-severe AD attending a university dermatology clinic had food hypersensitivity. 7 Other studies delineating the role of IgE-bearing antigen-presenting cells in establishing T H 2 lymphocytic responses 8 and demonstrating the predominant T H 2-lymphocytic infiltrate in acute eczematous lesions 9 have provided further support for the pathogenic role of allergy in AD.Animal models provide powerful tools for dissecting pathogenic mechanisms responsible for various disorders. A number of murine models of asthma have been developed in the past several years that have contributed greatly to our understanding of the immunopathogenesis of allergen-induced asthma. 10-12 Models of antigenassociated AD have been reported in cats and dogs, but because of difficulties with consistent induction of ADlike eruptions and high expense, they have not been widely studied. 13,14 A mouse strain, NC/Nga, has been reported that spontaneously has an AD-like skin lesion and IgE hyperproduction, presumably triggered by environmental factors. 15 More recently, a murine model of AD was described in which BALB/c mice were sensitized to ovalbumin (OVA...

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“…[43][44][45] It is widely known that the skin in atopic dermatitis is often colonized by Staphylococcus aureus strains that may generate a number of enterotoxins with super-antigenic capacity, such as Staphylococcal enterotoxins (SE)-A, SE-B , SE-C, SE-D, SE-E and toxic shock toxin 1 (TSST-1). [46][47][48][49][50][51][52] All these super-antigens may amplify the expression of skin-homing receptor (CLA) on T cells and induce the appearance of skewed T-cell clones. 47,48,52 For example, TSST-1 may stimulate selectively TCR-Vβ2-bearing cells, SE-C may bind both Vβ5.1 and Vβ13.1, SE-B and SE-C Vβ17 and SE-E Vβ5.1.…”

Section: Discussionmentioning

confidence: 99%

The role of 9-O-acetylated ganglioside D3 (CD60) and 4 1 (CD49d) expression in predicting the survival of patients with Sezary syndrome

Scala

Abeni²,

Pomponi³

et al. 2010

Haematologica

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BackgroundSézary syndrome is a rare and very aggressive leukemic variant of cutaneous T-cell lymphoma characterized by extensive skin involvement and a malignant circulating CD4 + T-cell clone which homes to the skin, over-expresses CD60, and lacks CD7, CD26 and CD49d. So far prognostic markers in this disease are limited to treatment with systemic steroids, age, serum lactate dehydrogenase, and a white blood cell count of 20¥10 9 /L or higher: no other biological marker with prognostic value, especially related to malignant cells, has been described. Design and MethodsWe used flow activated cell sorting analysis to compare the distribution of the T-cell receptor-Vβ repertoire and several surface molecules (CD7, CD26, CD49d and CD60) within the circulating CD4 + T-cell population in 62 patients with Sézary syndrome, 180 with mycosis fungoides, 6 with B-cell lymphomas, and 19 with chronic eczema. We calculated the 5-year overall survival of patients with Sézary syndrome after first hospital admission using Kaplan-Meier product-limit estimates and hazard ratios from the Cox proportional hazards model. ResultsWe found that both higher number of CD60 + and lower number of CD49d + cells within circulating CD4 + T cells at disease presentation were significantly associated with a lower probability of survival. An exceedingly high risk of death was observed for patients with a combination of a high proportion of CD4 /L) (hazard ratio = 12.303, 95% confidence interval 1.5-95.9; P<0.02). In addition, a skewed usage of T-cell receptor-Vβ subfamilies was observed in the circulating T-cell clone for 61.9% of all patients with Sézary syndrome, T-cell receptor-Vβ 2 and 5.1 subfamilies being the most frequently represented (42.8%), followed by T-cell receptor-Vβ 12 and 13.1. ConclusionsIn this study we showed that up-regulation of CD60 and down-regulation of CD49d on circulating CD4 + T cells are two useful markers for predicting a very poor outcome in patients with Sézary syndrome.Key words: TCR-Vβ repertoire, CD60, CD49d, survival rate, Sézary syndrome. Haematologica 2010;95(11):1905-1912. doi:10.3324/haematol.2010 This is an open-access paper.The role of 9-O-acetylated ganglioside D3 (CD60) and α4β1 (CD49d) expression in predicting the survival of patients with Sézary syndrome

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Evaluation of the staphylococcal exotoxins and their specific IgE in childhood atopic dermatitis☆☆☆

Cited by 134 publications

References 14 publications

Topical Superantigen Exposure Induces Epidermal Accumulation of CD8+ T Cells, a Mixed Th1/Th2-Type Dermatitis and Vigorous Production of IgE Antibodies in the Murine Model of Atopic Dermatitis

Topical Superantigen Exposure Induces Epidermal Accumulation of CD8+ T Cells, a Mixed Th1/Th2-Type Dermatitis and Vigorous Production of IgE Antibodies in the Murine Model of Atopic Dermatitis

Murine model of atopic dermatitis associated with food hypersensitivity

The role of 9-O-acetylated ganglioside D3 (CD60) and 4 1 (CD49d) expression in predicting the survival of patients with Sezary syndrome

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