{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T17:02:38Z","timestamp":1784739758810,"version":"3.55.0"},"reference-count":35,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T00:00:00Z","timestamp":1782432000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI141486"],"award-info":[{"award-number":["AI141486"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,7,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Basophils secrete histamine and IL-4\/13 when cocultured with human lung adenocarcinoma cells (A549 cells). Previous studies have revealed that this interaction is dependent on galectin-3 expression on the surface of A549 cells (EC-Gal-3), IgE present on the surface of IL-3 primed basophils, and direct physical interaction between the two cell types, indicating a cognate interaction between IgE and Gal-3. Reciprocal secretion of protumorigenic cytokines (IL-6\/VEGF-A) from A549 cells also results. Here, we further define the biological parameters required for this mode of activation. EC-Gal-3 stimulus has \u223c20-fold less IgE crosslinking capacity compared with standard anti-IgE. The capacity of IgE-bearing basophils to elicit an EC-Gal-3\u2013mediated response correlates with their responsiveness to standard anti-IgE stimulation, which is known to vary widely among individuals. However, unlike standard anti-IgE stimulation, basophil releasability in response to EC-Gal-3 is influenced by glycosylation patterns on surface-bound IgE. Specifically, bulk sialylation on IgE molecules suppress cellular releasability. Whole-cell basophil sialylation also suppresses EC-Gal-3 mediated activation. Gal-3 is an endogenous lectin with multivalent binding capacity and is implicated in a range of diseases involving immune modulation, organ fibrosis, and tumor metastasis. These results can help identify specific physiological and pathophysiological conditions by which IgE:Gal-3 interactions drive disease processes including wound healing, cancer, and fibrosis, including that which occurs in asthma.<\/jats:p>","DOI":"10.1093\/jleuko\/qiag087","type":"journal-article","created":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T11:50:51Z","timestamp":1782388251000},"source":"Crossref","is-referenced-by-count":0,"title":["Sialylation modulates basophil responsiveness to galectin-3\u2013dependent activation"],"prefix":"10.1093","volume":"118","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-6376-316X","authenticated-orcid":false,"given":"Laurent","family":"Ehrlich","sequence":"first","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins University , 5501 Hopkins Bayview Circle, Baltimore, MD 21224 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donald W","family":"MacGlashan","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins University , 5501 Hopkins Bayview Circle, Baltimore, MD 21224 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Anthony","sequence":"additional","affiliation":[{"name":"Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Charlestown, MA 02129 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle","family":"Conroy","sequence":"additional","affiliation":[{"name":"Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Charlestown, MA 02129 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anja P","family":"Bieneman","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins University , 5501 Hopkins Bayview Circle, Baltimore, MD 21224 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5263-7850","authenticated-orcid":false,"given":"John T","family":"Schroeder","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins University , 5501 Hopkins Bayview Circle, Baltimore, MD 21224 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2026,6,26]]},"reference":[{"key":"2026072212174606600_qiag087-B1","doi-asserted-by":"publisher","first-page":"855","DOI":"10.4049\/jimmunol.1700055","article-title":"Activation of human basophils by A549 lung epithelial cells reveals a novel IgE-dependent response independent of allergen","volume":"199","author":"Schroeder","year":"2017","journal-title":"J Immunol"},{"key":"2026072212174606600_qiag087-B2","doi-asserted-by":"publisher","first-page":"312","DOI":"10.1016\/j.jaci.2019.03.001","article-title":"Galectin-3 is essential for IgE-dependent activation of human basophils by A549 lung epithelial cells","volume":"144","author":"Schroeder","year":"2019","journal-title":"J Allergy Clin Immunol"},{"key":"2026072212174606600_qiag087-B3","doi-asserted-by":"publisher","first-page":"qiae233","DOI":"10.1093\/jleuko\/qiae233","article-title":"Basophils induce protumorigenic cytokines from A549 lung adenocarcinoma via mechanisms requiring IgE, galectin-3, and IL-3 priming","volume":"117","author":"Schroeder","year":"2025","journal-title":"J Leukoc Biol"},{"key":"2026072212174606600_qiag087-B4","doi-asserted-by":"publisher","first-page":"1548","DOI":"10.4049\/jimmunol.140.5.1548","article-title":"Modulation of phenotypic and functional properties of human peripheral blood monocytes by IL-4","volume":"140","author":"te Velde","year":"1988","journal-title":"J Immunol"},{"key":"2026072212174606600_qiag087-B5","doi-asserted-by":"publisher","first-page":"1808","DOI":"10.4049\/jimmunol.153.4.1808","article-title":"IgE-dependent IL-4 secretion by human basophils. 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