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Basophil Activation Test for Allergy Diagnosis
Published on: May 31, 2021
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In human basophils, IL-3 selectively induces RANKL expression that is modulated by IgER-dependent and
C Huber1, A Odermatt, B Hagmann
1Institute of Immunology, University Hospital Bern, Inselspital, Bern, Switzerland.
Allergy
|July 30, 2014
Summary
Interleukin-3 (IL-3) induces receptor activator of NF-κB ligand (RANKL) in human basophils, impacting immune cell activation and bone physiology. Stimuli modulate this RANKL expression, particularly in rheumatoid arthritis models.
Area of Science:
- Immunology
- Cell Biology
- Rheumatology
Background:
- Receptor activator of NF-κB ligand (RANKL) plays a role in immunoregulation and bone resorption, relevant to rheumatoid arthritis (RA).
- Activated basophils contribute to collagen-induced arthritis (CIA), a mouse model for RA.
- Understanding basophil RANKL expression is crucial for RA pathogenesis.
Purpose of the Study:
- To investigate the conditions under which human basophils express RANKL.
- To determine the role of Interleukin-3 (IL-3) and other stimuli in regulating RANKL expression in basophils.
Main Methods:
- Basophils were cultured with IL-3 and/or IgER-dependent/independent stimuli.
- RANKL protein and mRNA expression were analyzed using flow cytometry, ELISA, and real-time PCR.
- A coculture system assessed the biological activity of basophil-derived RANKL.
Main Results:
- IL-3 alone induced de novo expression of soluble and surface RANKL in human basophils.
- IgER cross-linking reduced surface RANKL expression upon simultaneous stimulation.
- Consecutive stimulation with IgER-dependent and independent stimuli enhanced RANKL expression, mainly at the mRNA level.
Conclusions:
- IL-3 is a potent inducer of RANKL in human basophils, linking them to bone physiology and immune cell activation.
- IgER-dependent and independent stimuli modulate IL-3-mediated RANKL expression in a time- and stimulus-dependent manner.
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