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Updated: Jun 27, 2026
13:36
Generation of Monocyte-Derived Dendritic Cells with Differing Sialylated Phenotypes
Published on: October 20, 2023
Sialylation modulates basophil responsiveness to galectin-3-dependent activation
Laurent Ehrlich1, Donald W MacGlashan1, Robert Anthony2
1Johns Hopkins Asthma and Allergy Center, Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins University, 5501 Hopkins Bayview Circle, Baltimore, MD 21224, United States.
Journal of Leukocyte Biology
|June 26, 2026
Summary
Lung adenocarcinoma cells activate basophils via IgE and Galectin-3. Glycosylation of IgE, particularly sialylation, impacts this interaction, influencing disease processes like cancer and fibrosis.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Basophils release histamine and cytokines upon interaction with lung adenocarcinoma cells (A549).
- This interaction involves surface Galectin-3 (Gal-3) on A549 cells and IgE on basophils, leading to reciprocal cytokine secretion.
- Gal-3 is implicated in immune modulation, fibrosis, and tumor metastasis.
Purpose of the Study:
- To further define the biological parameters governing IgE:Gal-3 mediated basophil activation.
- To investigate the role of IgE glycosylation in this cellular interaction.
- To understand the implications for disease processes.
Main Methods:
- Co-culture of A549 cells with IL-3 primed basophils.
- Stimulation with engineered A549 cells expressing Gal-3 (EC-Gal-3) and standard anti-IgE.
- Analysis of basophil releasability and IgE cross-linking capacity.
- Assessment of IgE glycosylation patterns, including sialylation.
Main Results:
- EC-Gal-3 exhibits significantly lower IgE cross-linking capacity than anti-IgE.
- Basophil responsiveness to EC-Gal-3 correlates with responsiveness to anti-IgE but is modulated by IgE glycosylation.
- Increased sialylation on IgE molecules suppresses basophil releasability and EC-Gal-3 mediated activation.
- Whole cell basophil sialylation also inhibits EC-Gal-3 activation.
Conclusions:
- IgE:Gal-3 interactions are a distinct mechanism of basophil activation, influenced by IgE glycosylation.
- Sialylation of IgE acts as a negative regulator of basophil activation in this context.
- Understanding these interactions can inform strategies for diseases involving cancer, fibrosis, and asthma.
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