Flow cytometric basophil activation tests: Staining of exteriorized basophil granule matrix by fluorescent avidin versus appearance of CD63.


Journal

Cytometry. Part B, Clinical cytometry
ISSN: 1552-4957
Titre abrégé: Cytometry B Clin Cytom
Pays: United States
ID NLM: 101235690

Informations de publication

Date de publication:
11 2020
Historique:
received: 09 12 2019
revised: 06 01 2020
accepted: 10 01 2020
pubmed: 6 2 2020
medline: 20 8 2021
entrez: 4 2 2020
Statut: ppublish

Résumé

Staining of exteriorized basophil granule matrix by fluorescent avidin might be a reliable technique to monitor basophil degranulation. This study compares the avidin-based technique with the upregulation of CD203c and appearance of CD63 in response to various stimuli. Fourteen individuals responsive to anti-IgE, nine healthy controls, and five birch pollen-allergic patients, and five nonresponders were studied. Activation experiments included anti-IgE, fMLP, interleukin-(IL)-3, and birch pollen allergen. Basophil activation/degranulation was analyzed by flow cytometry and microscopy using anti-CD63, anti-CD203c, and avidin. Stimulation with anti-IgE, fMLP, and relevant allergen results in upregulation of CD203c, CD63 appearance, and an increase in avidin binding. In response to anti-IgE and allergen, upregulation of CD203c peaks within 10 min, CD63 and avidin binding reach a plateau after 10-20 min. CD63 staining leads to a bimodal distribution, avidin staining causes a unimodal shift with a less clear discrimination between degranulating and nondegranulating cells. In response to fMLP, upregulation of CD203c and CD63 and avidin binding are maximal after 2.5 min. Following incubation with anti-IgE and fMLP, percentages of CD203c+ cells are higher than those of CD63+ and avidin+ cells, pointing to a dissociation between activation and degranulation. Percentages of CD63+ cells are systemically higher than those of avidin+ cells. Incubated with IL-3 only upregulates CD203c, while no CD63 or avidin binding is observed. Staining of exteriorized proteoglycans by avidin is a reliable technique to quantify basophil degranulation but offers no added value when compared to traditional assays that use CD63 as a readout.

Sections du résumé

BACKGROUND
Staining of exteriorized basophil granule matrix by fluorescent avidin might be a reliable technique to monitor basophil degranulation. This study compares the avidin-based technique with the upregulation of CD203c and appearance of CD63 in response to various stimuli.
METHODS
Fourteen individuals responsive to anti-IgE, nine healthy controls, and five birch pollen-allergic patients, and five nonresponders were studied. Activation experiments included anti-IgE, fMLP, interleukin-(IL)-3, and birch pollen allergen. Basophil activation/degranulation was analyzed by flow cytometry and microscopy using anti-CD63, anti-CD203c, and avidin.
RESULTS
Stimulation with anti-IgE, fMLP, and relevant allergen results in upregulation of CD203c, CD63 appearance, and an increase in avidin binding. In response to anti-IgE and allergen, upregulation of CD203c peaks within 10 min, CD63 and avidin binding reach a plateau after 10-20 min. CD63 staining leads to a bimodal distribution, avidin staining causes a unimodal shift with a less clear discrimination between degranulating and nondegranulating cells. In response to fMLP, upregulation of CD203c and CD63 and avidin binding are maximal after 2.5 min. Following incubation with anti-IgE and fMLP, percentages of CD203c+ cells are higher than those of CD63+ and avidin+ cells, pointing to a dissociation between activation and degranulation. Percentages of CD63+ cells are systemically higher than those of avidin+ cells. Incubated with IL-3 only upregulates CD203c, while no CD63 or avidin binding is observed.
CONCLUSIONS
Staining of exteriorized proteoglycans by avidin is a reliable technique to quantify basophil degranulation but offers no added value when compared to traditional assays that use CD63 as a readout.

Identifiants

pubmed: 32012452
doi: 10.1002/cyto.b.21868
doi:

Substances chimiques

Tetraspanin 30 0
Avidin 1405-69-2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

483-490

Informations de copyright

© 2020 International Clinical Cytometry Society.

Références

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Knol, E. F., Koenderman, L., Mul, F. P., Verhoeven, A. J., & Roos, D. (1991). Differential activation of human basophils by anti-IgE and formyl-methionyl-leucyl-phenylalanine. Indications for protein kinase C-dependent and -independent activation pathways. European Journal of Immunology, 21(4), 881-885.
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MacGlashan, D., Jr. (2010). Expression of CD203c and CD63 in human basophils: relationship to differential regulation of piecemeal and anaphylactic degranulation processes. Clinical and Experimental Allergy: Journal of the British Society for Allergy and Clinical Immunology., 40(9), 1365-1377.
Mukai, K., Chinthrajah, R. S., Nadeau, K. C., Tsai, M., Gaudenzio, N., & Galli, S. J. (2017). A new fluorescent-avidin-based method for quantifying basophil activation in whole blood. The Journal of Allergy and Clinical Immunology, 140(4), 1202-1206.e1203.
Mukai, K., Gaudenzio, N., Gupta, S., Vivanco, N., Bendall, S. C., Maecker, H. T., … Galli, S. J. (2017). Assessing basophil activation by using flow cytometry and mass cytometry in blood stored 24 hours before analysis. The Journal of Allergy and Clinical Immunology, 139(3), 889-899.e811.
Ronnberg, E., Melo, F. R., & Pejler, G. (2012). Mast cell proteoglycans. The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society., 60(12), 950-962.
Sabato, V., Verweij, M. M., Bridts, C. H., Levi-Schaffer, F., Gibbs, B. F., De Clerck, L. S., … Ebo, D. G. (2012). CD300a is expressed on human basophils and seems to inhibit IgE/FcepsilonRI-dependent anaphylactic degranulation. Cytometry Part B, Clinical Cytometry, 82(3), 132-138.
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Auteurs

Didier G Ebo (DG)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Research Consortium of Excellence, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium.
Department of Immunology and Allergology, AZ Jan Palfijn Gent, Ghent, Belgium.

Jessy Elst (J)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Research Consortium of Excellence, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium.

Michel van Houdt (M)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Research Consortium of Excellence, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium.

Isabel Pintelon (I)

Laboratory of Cell Biology and Histology, Department of Veterinary Sciences, University of Antwerp, Antwerp, Belgium.

Jean-Pierre Timmermans (JP)

Laboratory of Cell Biology and Histology, Department of Veterinary Sciences, University of Antwerp, Antwerp, Belgium.

Tatsuo Horiuchi (T)

Department of Anesthesiology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.

Margaretha A Faber (MA)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Research Consortium of Excellence, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium.

Margo M Hagendorens (MM)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Research Consortium of Excellence, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium.
Department of Pediatrics, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium.

Christel M Mertens (CM)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Research Consortium of Excellence, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium.

Vito Sabato (V)

Department of Immunology, Allergology, Rheumatology and the Infla-Med Research Consortium of Excellence, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium.
Department of Immunology and Allergology, AZ Jan Palfijn Gent, Ghent, Belgium.

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