In vivo expression of IL-12 and IL-13 in atopic dermatitis

Hamid, Qutayba; Naseer, Tanveer; Minshall, Eleanor; Song, Yu; Boguniewicz, Mark; Leung, Donald Y.M.

doi:10.1016/s0091-6749(96)70246-4

Cited by 338 publications

(241 citation statements)

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“…This is similar to findings reported in human subjects with AD. 9,41 These findings differ from the histopathologic findings in patients with chronic urticaria, in whom mast cell numbers (predominantly perivascular) are reportedly increased 10-fold, and the increased numbers of infiltrating lymphocytes show no predominance of CD4 + or CD8 + lymphocytes. 42 The presence of increased numbers of eosinophils in the skin and peripheral blood, increased cutaneous mast cells, and elevated levels of serum IgE antibodies are consistent with the predominantly T H 2 response seen in AD in human subjects.…”

Section: Discussionmentioning

confidence: 71%

Murine model of atopic dermatitis associated with food hypersensitivity

Kleiner²,

Huang³

et al. 2001

Journal of Allergy and Clinical Immunology

109

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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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Section: Discussionmentioning

confidence: 71%

Murine model of atopic dermatitis associated with food hypersensitivity

Kleiner²,

Huang³

et al. 2001

Journal of Allergy and Clinical Immunology

109

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“…T-cell expression of IL-4, IL-5, and IL-13 is significantly upregulated in both acute and chronic AD lesions, as compared to nonlesional AD skin and healthy skin (35,36). Based on atopy patch testing using house dust mite allergens, a biphasic model of cytokine expression by T cells in AD was observed: an initial increase in the infiltration of IL-4 + T cells into AD lesions, followed by infiltration of IFN-γ + T cells in the chronic phase (37).…”

Section: Adaptive Immunity: Perpetrator Of Persistent and Chronic Infmentioning

confidence: 99%

New insights in the pathogenesis of atopic dermatitis

Ong

2013

Pediatr Res

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“…In patients with AD and allergy toward inhalation allergens, such as house dust mite, circulating allergen-specific T H 2 cells have shown to be important in the pathogenesis of allergic skin symptoms. [2][3][4] The infiltration into the skin of these T cells, which produce high levels of IL-4, IL-5, and IL-13 but little or no IFN-γ, 5,6 can mediate allergic skin inflammation through stimulation of IgE synthesis and eosinophil recruitment. 7 Evidence for these mechanisms in food allergy is much less well established.…”

mentioning

confidence: 99%