Now we have beforehand proven that human basophils launch mediators (histamine, IL-4, IL-13) when co-cultured with epithelial/most cancers cells expressing galectin-3 (EC-GaL-3) –a lectin lengthy identified to bind IgE. This response depends on basophils expressing IgE and requires cognate interplay with EC-GAL-3. Provided that monocytes are implicated as a supply of Gal-3, and that basophil-derived cytokines (IL-4/IL-13) drive the M2-like phenotype (in vitro & in vivo), we now hypothesize that basophils promote Gal-3 manufacturing by M2-like cells.
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