Immunoglobulin E in Dermatoses

Juhlin, Lennart; Johansson, S. G. O.; Bennich, H.; Högman, Claes F.; Thyresson, N

doi:10.1001/archderm.1969.01610250018004

Cited by 241 publications

(48 citation statements)

References 9 publications

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“…The low incidence of high IgE in drug eruptions other than urticaria corresponds well with the results of Juhlin et al [20] and Brehm [6], According to Ackroyd and Rook [1], there is no conclusive evidence that patients who have a history of atopy develop drug reactions more frequently than normal individuals. Our observation that only 4 of 21 drug-allergic patients with high IgE had a history of atopy confirms this opinion.…”

Section: Discussionsupporting

confidence: 83%

IgE in Allergic Drug Reactions

Müller¹,

Morell²,

Hoigné³

1973

Int Arch Allergy Immunol

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Sera of 102 patients with allergic drug reactions were investigated for IgE levels by radioactive single radial immunodiffusion. High IgE serum concentrations were more frequently found in these patients than in a control group of healthy blood donors. Most of the elevated IgE levels were seen in patients with urticaria or anaphylactic shock (type I reactions). One third of these patients had raised IgE compared to only 6% of the control group. In patients with maculopapular rashes and in type III reactions (Arthus reaction, serum sickness, etc.), the incidence of high IgE was not significantly increased. Surprisingly, elevated IgE was often found in thrombocytopenia and agranulocytosis (type II reactions).

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Section: Discussionsupporting

confidence: 83%

IgE in Allergic Drug Reactions

Müller¹,

Morell²,

Hoigné³

1973

Int Arch Allergy Immunol

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“…For example, the histology of AD shares many features with classic allergic contact delayed-type hypersensitivity, including spongiosis and a dominant T cell inflammatory infiltrate that is distributed predominantly in a dermal, and to a lesser extent epidermal pattern. Approximately 80% of individuals with AD have circulating specific IgE recognizing one or more of house dust mite, cat, dog, grass, and other ubiquitous environmental allergens (1). In many studies, allergen-specific CD4 ϩ and CD8 ϩ T cells have been documented to be present in the peripheral blood and lesional skin of affected individuals and to produce diverse cytokines but with a frequent T helper 2 (Th2) dominance (2,3).…”

Section: Atopy ͉ T Cells ͉ Keratinocytes ͉ Staphylococcusmentioning

confidence: 99%

Bacterial superantigen facilitates epithelial presentation of allergen to T helper 2 cells

Ardern‐Jones

Black

Bateman

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Although clinical and laboratory evidence support roles for both staphylococcal infection and environmental allergens in the pathogenesis of atopic dermatitis, human studies have largely considered these variables independently. We sought to test the hypothesis that staphylococcal superantigen influences the allergen-specific T cell response. We first mapped a Der p 1 epitope and used HLA DRB1*1501 class II tetramer-based cell sorted populations to show that specific CD4 ؉ T cells were able to recognize the peptide presented by HLA DR-matched keratinocytes. We observed that staphylococcal enterotoxin B (SEB) enhanced the IL-4 Der p 1-specific T cell response. This response was mediated by two synergistic mechanisms: first, SEB-induced IFN-␥ promoted class II and intercellular adhesion molecule-1 expression by presenting keratinocytes; and second, SEB-induced IL-4 directly amplified allergen-specific CD4 ؉ T cell production of many cytokines. We propose that handling of staphylococcal infection is a critical step in the amplification of the allergen-specific T cell response, linking two common disease associations and with implications for the prevention and treatment of atopic disease.T here is convincing evidence that allergic reactivity to environmental challenge has a role in the pathogenesis of atopic dermatitis (AD). For example, the histology of AD shares many features with classic allergic contact delayed-type hypersensitivity, including spongiosis and a dominant T cell inflammatory infiltrate that is distributed predominantly in a dermal, and to a lesser extent epidermal pattern. Approximately 80% of individuals with AD have circulating specific IgE recognizing one or more of house dust mite, cat, dog, grass, and other ubiquitous environmental allergens (1). In many studies, allergen-specific CD4 ϩ and CD8 ϩ T cells have been documented to be present in the peripheral blood and lesional skin of affected individuals and to produce diverse cytokines but with a frequent T helper 2 (Th2) dominance (2, 3). House dust mite extract application to the skin of individuals with AD can reproduce eczematous changes (4, 5), and allergen avoidance has been shown by some to be partially effective (6, 7). Keratinocytes have been shown to up-regulate HLA class II and intercellular adhesion molecule-1 (ICAM-1) in AD and other inflammatory dermatoses (8, 9) and also in response to injection of IFN-␥ into normal skin (10). However, in isolation, allergic reactivity to an environmental challenge does not explain all of the features of AD. Twenty percent of affected individuals do not generate IgE responses to such ubiquitous proteins, and it is unclear why disease incidence changes during age and between different geographical regions. The risk of disease is clearly influenced by genetic susceptibility factors, some of which affect the immune response, e.g., polymorphisms of the Fc R1 and IL-4R genes (11-13). However, it is becoming increasingly clear from the genetic studies that skin-specific genes, determining variables s...

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“…Studies on patients with atopic dermatitis (AD) have revealed a variety of immunological, hormonal and psy chological [1,2] derangements including elevations of IgE levels [3,4], disordered cell-mediated immunity [5][6][7], abnormal cAMP and cAMP-phosphodiesterase activity [8,9] and an impairment of (1-adrenoceptor function [10,11]. Recent investigations pointed to a possible hormonal dysregulation of the hypothalamic-pituitary-adrenal (HPA) system in AD.…”

Section: Introductionmentioning

confidence: 99%

Elevated Glucocorticoid Receptor Concentrations before and after Glucocorticoid Therapy in Peripheral Mononuclear Leukocytes of Patients with Atopic Dermatitis

Rupprecht

Rupprecht²,

Kornhuber³

et al. 1991

Dermatology

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The number and affinity of glucocorticoid binding sites in peripheral mononuclear leukocytes of patients with atopic dermatitis (AD) and healthy controls were determined under baseline conditions and after a defined oral glucocorticoid treatment. Patients with AD (n = 15) exhibited significantly more glucocorticoid receptors (GR) per cell than the control group (n = 22), while the GR affinity did not differ. Methylprednisolone treatment resulted in a significant reduction of the GR sites per cell in the steroid-treated control group (n = 10) in contrast to the patients. The dissociation constant was not affected by methylprednisolone treatment in either group. In view of the therapeutic efficiency of glucocorticoids in AD and findings of abnormal cAMP and cAMP-phosphodiesterase activity, the elevated GR concentrations in AD lend support to the hypothesis of a compensatory GR upregulation due to an insufficient action of endogenous cortisol or to altered cAMP-induced GR expression.

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Immunoglobulin E in Dermatoses

Cited by 241 publications

References 9 publications

IgE in Allergic Drug Reactions

IgE in Allergic Drug Reactions

Bacterial superantigen facilitates epithelial presentation of allergen to T helper 2 cells

Elevated Glucocorticoid Receptor Concentrations before and after Glucocorticoid Therapy in Peripheral Mononuclear Leukocytes of Patients with Atopic Dermatitis

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