Immunoglobulin E in dermatoses. Levels in atopic dermatitis and urticaria

Juhlin, Lennart

doi:10.1001/archderm.100.1.12

Cited by 130 publications

(68 citation statements)

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“…The fact that only five patients had active lesions when studied may explain our failure to demonstrate the previously reported decrease in the number of basophils present in chronic urticaria patients (23). We do not believe that the unresponsiveness is due to low concentrations of IgE since, in contrast to previously reported results (24), the patients had significantly higher IgE levels than controls.…”

Section: Resultscontrasting

confidence: 99%

Defective histamine release in chronic urticaria.

Kern¹,

Lichtenstein²

1976

J. Clin. Invest.

145

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A B S T R A C T Histamine release from peripheral blood leukocytes challenged with anti-human IgE was studied in patients with chronic urticaria and nonatopic controls. 19 of 23 controls, but only 6 of 20 patients, released over 20% of the total available leukocyte histamine. The response to anti-IgE concentrations of 1.66, 0.33, 0.066, and 0.013 jAg antibody N/ml was significantly lower in patients than in controls. Serum IgE levels were significantly higher in the patients but total histamine content of about 107 leukocytes was not. Deuterium oxide (D20) greatly increased histamine release (in both groups), indicating that the anti-IgE interacted with the basophils of urticaria patients. Passive sensitization of leukocytes with biologically active IgE was achieved in both patients and control subjects whose cells responded to anti-IgE, but was not achieved in either patients or control subjects whose cells were nonresponsive to anti-IgE challenge. PI-anti-IgE autoradiographic studies revealed no obvious quantitative abnormality in the amount of basophil-bound IgE in chronic urticaria patients. Ionophore stimulation of aliquots of the same leukocytes used for anti-IgE challenge demonstrated that the urticaria patients' basophils were capable of releasing normal amounts of histamine. Leukocyte cyclic AMP levels in the two groups were not significantly different either in base-line levels or in responsiveness to stimulation with isoproterenol. These data indicate that chronic urticaria patients have a (acquired?) defect in leukocyte histamine release that occurs after the anti-IgE-IgE interaction, but before the actual (second-stage) release process, and that is comparable to the phenomenon of desensitization.

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Section: Resultscontrasting

confidence: 99%

Defective histamine release in chronic urticaria.

Kern¹,

Lichtenstein²

1976

J. Clin. Invest.

145

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“…For analysis of V H genes a set of 5 0 primers specific for human V H 1/V H 5/V H 7, V H 2, V H 3, V H 4 and V H 6 gene families containing a PstI restriction site [12] in combination with a 3 0 primer specific for the first exon of the constant region (position 134-139) [1] containing a SalI restriction site was employed (Fig. 1).…”

Section: Amplification Of V H Genesmentioning

confidence: 99%

“…Furthermore, in a high percentage of atopic patients serum IgE reactivity to a variety of environmental allergens [1] is accompanied by positive intracutaneous skin test reactions to one or more of these antigens [2].…”

Section: Introductionmentioning

confidence: 99%

VH genes expressed in peripheral blood IgE-producing B cells from patients with atopic dermatitis

Tilgner

Golembowski

Kersten

et al. 1997

Clinical and Experimental Immunology

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SUMMARYIn this study we analysed the V H genes expressed in IgE-producing peripheral B cells in two patients with severe atopic dermatitis. We found a diverse antibody repertoire containing V H genes of five different V H families, no V H 2 and 7 genes, with no biased usage of one particular V H gene family. Some V H germ-line segments were found to be used several times within the e transcripts (V3-23, V3-30).Comparison of the IgE-encoding V H genes with the respective germ-line elements revealed the expression of nearly germ-line identical as well as somatically mutated V H genes. In these latter V H genes base substitutions were distributed over both complementarity determining and framework regions. Because of the similarities between the IgE committed B cell repertoire in atopic patients and the peripheral B cell repertoire in non-atopic individuals we conclude that the atopic V H gene repertoire probably reflects the result of an increased class switch of polyclonal B cells, including virgin and mature B cells, in response to a Th2 cytokine profile.

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“…It affects 10-20% of children in developed countries and shows strong familial aggregation. 5 Eighty percent of patients with AD cases show elevated total serum IgE levels, 6 and atopic mechanisms dominate our current understanding of the pathogenesis of AD. 7 Serine protease inhibitor Kazal-type 5 (SPINK5) is responsible for Netherton syndrome, 8 a rare recessive skin disorder that is accompanied by atopy.…”

mentioning

confidence: 99%

Association between polymorphisms in the SPINK5 gene and atopic dermatitis in the Japanese

et al. 2003

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Atopy, which is characterized by increased levels of immunoglobulin E (IgE) against common environmental allergens, is considered the strongest predisposing factor for asthma and atopic dermatitis (AD). Mutations in the gene encoding serine protease inhibitor Kazal-type 5 (SPINK5) are responsible for Netherton syndrome, a rare skin disorder characterized by greatly elevated IgE levels with atopic manifestations. A recent study of Caucasian AD families showed that maternally derived alleles of the SPINK5 gene are associated with development of AD and asthma, suggesting the parent-of-origin effect for the development of atopic diseases in the SPINK5 gene. We studied the possible association of the SPINK5 gene for the development of atopic diseases by determining the genotypes of five polymorphisms in a Japanese population. Ttransmission disequilibrium tests revealed an association of SPINK5 polymorphisms with AD but not with asthma. Our data indicate that the SPINK5 gene is associated with AD across ethnicities.

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Immunoglobulin E in dermatoses. Levels in atopic dermatitis and urticaria

Cited by 130 publications

References 0 publications

Defective histamine release in chronic urticaria.

Defective histamine release in chronic urticaria.

VH genes expressed in peripheral blood IgE-producing B cells from patients with atopic dermatitis

Association between polymorphisms in the SPINK5 gene and atopic dermatitis in the Japanese

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