IL3 effect on basophils histamine release upon stimulation with chronic urticaria sera

Background:  Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to releas...

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Published inAllergy (Copenhagen) Vol. 58; no. 8; pp. 802 - 807
Main Authors Ferrer, M., Luquin, E., Kaplan, A. P.
Format Journal Article
LanguageEnglish
Published Oxford, UK Munksgaard International Publishers 01.08.2003
Blackwell
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Abstract Background:  Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay. Methods:  We incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a ‘non‐releaser’ with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement. Results:  Interleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse ‘non‐releaser’ basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen. Conclusions:  Preincubating basophils with IL3 facilitates the identification of sera with anti‐IgE receptor antibody but does not affect the percentage of sera designated as positive.
AbstractList Background:  Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay. Methods:  We incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a ‘non‐releaser’ with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement. Results:  Interleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse ‘non‐releaser’ basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen. Conclusions:  Preincubating basophils with IL3 facilitates the identification of sera with anti‐IgE receptor antibody but does not affect the percentage of sera designated as positive.
BACKGROUNDChronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay.METHODSWe incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a 'non-releaser' with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement.RESULTSInterleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse 'non-releaser' basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen.CONCLUSIONSPreincubating basophils with IL3 facilitates the identification of sera with anti-IgE receptor antibody but does not affect the percentage of sera designated as positive.
Background: Chronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay. Methods: We incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a `non-releaser' with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement. Results: Interleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse `non-releaser' basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen. Conclusions: Preincubating basophils with IL3 facilitates the identification of sera with anti-IgE receptor antibody but does not affect the percentage of sera designated as positive.
Chronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay. We incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a 'non-releaser' with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement. Interleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse 'non-releaser' basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen. Preincubating basophils with IL3 facilitates the identification of sera with anti-IgE receptor antibody but does not affect the percentage of sera designated as positive.
Background:  Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the IgE receptor. Patients possessing this antibody are identified by the ability of serum to degranulate donor basophils to release histamine. We questioned whether priming of basophils with interleukin 3 (IL3) would facilitate identification of patients and/or alter the percentage of patients who have a positive assay. Methods:  We incubated 37 chronic urticaria sera with basophils from donors with no urticaria with and without priming with IL3 and compared histamine release in each instance. We also preincubated basophils from a ‘non‐releaser’ with IL3, used these cells to assay chronic urticaria sera, and assessed the contribution of complement. Results:  Interleukin 3 increases the amount of histamine release by the sera which is able to activate basophils, but it does not convert negative sera into positive releasers. Interleukin 3 is able to partially reverse ‘non‐releaser’ basophils into cells that respond to chronic urticaria sera, and complement cannot account for the augmentation seen. Conclusions:  Preincubating basophils with IL3 facilitates the identification of sera with anti‐IgE receptor antibody but does not affect the percentage of sera designated as positive.
Author Ferrer, M.
Kaplan, A. P.
Luquin, E.
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Issue 8
Keywords Human
Immunopathology
Skin disease
Urticaria
basophils; IgE receptor
IgE
Cytokine
Granulocyte
Immunoglobulin receptor
Basophil
Histamine
Interleukin 3
IL3; urticaria
Language English
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Snippet Background:  Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody...
Chronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody reactive with the...
Background:  Chronic urticaria is thought to be an autoimmune disorder in 35–40% of patients because of the presence of an immunoglobulin G (IgG) antibody...
Background: Chronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody...
BACKGROUNDChronic urticaria is thought to be an autoimmune disorder in 35-40% of patients because of the presence of an immunoglobulin G (IgG) antibody...
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SubjectTerms Adult
Allergic diseases
basophils
Basophils - metabolism
Biological and medical sciences
Chronic Disease
Female
histamine
Histamine Release - drug effects
Humans
IgE receptor
IL3
Immunopathology
In Vitro Techniques
Interleukin-3 - pharmacology
Male
Medical sciences
Skin allergic diseases. Stinging insect allergies
urticaria
Urticaria - blood
Title IL3 effect on basophils histamine release upon stimulation with chronic urticaria sera
URI https://onlinelibrary.wiley.com/doi/abs/10.1034%2Fj.1398-9995.2003.00195.x
https://www.ncbi.nlm.nih.gov/pubmed/12859562
https://search.proquest.com/docview/18941390
https://search.proquest.com/docview/73464409
Volume 58
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