Increased release of histamine by anti‐IgE from leucocytes of asthmatic patients and possible heterogeneity of IgE

Assem, E. S. K.; Attallah, N.A.

doi:10.1111/j.1365-2222.1981.tb01607.x

Cited by 30 publications

(12 citation statements)

References 8 publications

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“…In summary, our data strongly support the exis tence of some kind of heterogeneity in IgE proteins as previously suggested by histamine release experi ments [30][31][32] and differences in complement-fixing properties [33]. Moreover, it is noteworthy that IgM and IgG anti-IgE Ab can be of different specificities which should be considered when interpreting such data.…”

Section: Discussionsupporting

confidence: 64%

Autoantibodies of the IgM Class against a Human Myeloma Protein IgE(DES). II. Specificity

Magnusson

Vaerman

1986

Int Arch Allergy Immunol

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Five different monoclonal IgE proteins, papain and pepsin fragments of myeloma protein IgE(DES) and particle-counting immunoassay were used to study in detail the epitope(s) of IgE(DES) involved in the agglutination with IgM anti-IgE(DES) antibodies. The specificity of these autoantibodies was restricted to IgE(DES) as they did not react with latex particles coated with four other IgE myeloma proteins. Antibodies reactive with latex-IgE other than latex-IgE(DES), when present, were also of restricted specificity as shown by criss-cross absorption experiments. These differences between IgE myeloma proteins could not be attributed to the light chain type nor to the Em(l)-allotype. The epitope(s) of IgE(DES) participating in the reaction was heat-resistant (56 °C, 2 h) and localized in the pepsin F(ab′)_2ε fragment, but was absent in the papain Fc_ε and Fab_ε fragments. Further degradation by pepsin of the F(ab′)_2ε fragment (molecular weight 145,000 daltons) to 5S_ε (90,000 daltons) and Fc_εXXX fragments (30,000 daltons) destroyed the reacting epitope. These results indicate that the IgM antibodies were not directed against k chain or idiotypic determinants of IgE(DES), but to some epitope(s) in the undegraded hinge region. Therefore, it seems that some kind of antigenic heterogeneity, perhaps related to the carbohydrate moieties, is present in IgE myeloma proteins besides the known idiotypic, allotypic and isotypic ones.

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Section: Discussionsupporting

confidence: 64%

Autoantibodies of the IgM Class against a Human Myeloma Protein IgE(DES). II. Specificity

Magnusson

Vaerman

1986

Int Arch Allergy Immunol

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“…Previous groups have reported both increases and decreases in FcRI-mediated degranulation when basophils are isolated from asthmatics (21)(22)(23)(24). These data have contributed to the longstanding controversy over the role of basophils in asthma (reviewed in Ref.…”

Section: Discussionmentioning

confidence: 99%

Histamine Release from the Basophils of Control and Asthmatic Subjects and a Comparison of Gene Expression between “Releaser” and “Nonreleaser” Basophils

Youssef

Schuyler²,

Gilmartin

et al. 2007

The Journal of Immunology

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Most human blood basophils respond to FcεRI cross-linking by releasing histamine and other inflammatory mediators. Basophils that do not degranulate after anti-IgE challenge, known as “nonreleaser” basophils, characteristically have no or barely detectable levels of the Syk tyrosine kinase. The true incidence of the nonreleaser phenotype, its relationship (if any) to allergic asthma, and its molecular mechanism are not well understood. In this study, we report statistical analyses of degranulation assays performed in 68 control and 61 asthmatic subjects that establish higher basal and anti-IgE-stimulated basophil degranulation among the asthmatics. Remarkably, 28% of the control group and 13% of the asthmatic group were nonreleasers for all or part of our 4-year long study and cycling between the releaser and nonreleaser phenotypes occurred at least once in blood basophils from 8 (of 8) asthmatic and 16 (of 23) control donors. Microarray analysis showed that basal gene expression was generally lower in nonreleaser than releaser basophils. In releaser cells, FcεRI cross-linking up-regulated >200 genes, including genes encoding receptors (the FcεRI α and β subunits, the histamine 4 receptor, the chemokine (C-C motif) receptor 1), signaling proteins (Lyn), chemokines (IL-8, RANTES, MIP-1α, and MIP-1β) and transcription factors (early growth response-1, early growth response-3, and AP-1). FcεRI cross-linking induced fewer, and quite distinct, transcriptional responses in nonreleaser cells. We conclude that “nonreleaser” and “cycler” basophils represent a distinct and reversible natural phenotype. Although histamine is more readily released from basophils isolated from asthmatics than controls, the presence of nonreleaser basophils does not rule out the diagnosis of asthma.

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“…Basophil releasability is increased in patients with allergic rhinitis and asthma [5][6][7], and it has been suggested that it may contribute to the pathogenesis of allergic disease. LICHTENSTEIN and co-workers [8] showed that the severity of symptoms in allergic patients during the ragweed season correlated with basophil sensitivity to antigen stimulation in vitro.…”

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confidence: 99%

Defective inhibition of sodium on basophil histamine release in patients with allergic rhinitis and bronchial asthma

Tedeschi¹,

Cottini²,

Salmaso³

et al. 1996

Eur Respir J

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D De ef fe ec ct ti iv ve e i in nh hi ib bi it ti io on n o of f s so od di iu um m o on n b ba as so op ph hi il l h hi is st ta am mi in ne e r re el le ea as se e i in n p pa at ti ie en nt ts s w wi it th h a al ll le er rg gi ic c r rh hi in ni it ti is s a an nd d b br ro on nc ch hi ia al l a as st th hm ma a A. Tedeschi*, M. Cottini**, C. Salmaso*, N. Milazzo*, A. Miadonna* Defective inhibition of sodium on basophil histamine release in patients with allergic rhinitis and bronchial asthma. A. Tedeschi, M. Cottini, C. Salmaso, N. Milazzo, A. Miadonna. ©ERS Journals Ltd 1996. ABSTRACT: The aim of this study was to evaluate whether Na + exerts its inhibitory effect on basophil histamine release induced by immunoglobulin E (IgE)-dependent (anti-IgE) and IgE-independent (N-formyl-methionyl-leucyl-phenylalanine (FMLP), interleukin-3 (IL-3)) stimuli in patients with allergic rhinitis (n=24) and allergic bronchial asthma (n=10). Peripheral blood leucocytes were stimulated with anti-IgE, FMLP and IL-3 in the presence of high and low Na + concentrations, and histamine release was measured using a fluorometric method.In standard Na + -containing medium, spontaneous and stimulated histamine release was higher in allergic patients (n=34) (both rhinitic and asthmatic) than in healthy subjects (n=41). Na + removal from extracellular medium and its isosmotic substitution with choline chloride or with N-methyl-D-glucamine led to a significant increase of anti-IgE-, FMLP-and IL-3-induced histamine release in normal subjects, but not in allergic patients. The increase in Na + concentration in the extracellular medium was accompanied by a dose-dependent decrease of anti-IgE-and FMLP-induced histamine release in normal subjects, but not in allergic patients. The behaviour of atopics and healthy subjects was different and not related to the basophil responsiveness to activating signals. The incubation of basophils from healthy subjects with sera from allergic patients did not have a significant influence on the inhibitory effect of Na + .Basophils from healthy subjects and atopic patients respond differently when stimulated in a low Na + medium. The reduced sensitivity to the inhibitory effect of Na + may contribute to basophil dysfunction in patients with respiratory allergy.

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Increased release of histamine by anti‐IgE from leucocytes of asthmatic patients and possible heterogeneity of IgE

Cited by 30 publications

References 8 publications

Autoantibodies of the IgM Class against a Human Myeloma Protein IgE(DES). II. Specificity

Autoantibodies of the IgM Class against a Human Myeloma Protein IgE(DES). II. Specificity

Histamine Release from the Basophils of Control and Asthmatic Subjects and a Comparison of Gene Expression between “Releaser” and “Nonreleaser” Basophils

Defective inhibition of sodium on basophil histamine release in patients with allergic rhinitis and bronchial asthma

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