Fig. 2. Mechanisms of recruitment and functions of basophils in the TME. (a) Basophils were recruited and activated in TDLNs under the influence of TME, and regulated the tumor-promoting Th2 immune response in PDAC. The recruitment of basophils into TDLN was closely associated with the secretion of chemokines CCL7/MCP3 by M2 macrophages, and basophil activation was induced by T cell-derived IL-3. (b) Treg depletion in melanoma-bearing mice enhanced tumor infiltration of basophils and CD8⁺ T cells, leading to the rejection of the tumor. Intratumoral basophils enhanced CD8⁺ T cell accumulation via the production of chemokines CCL3 and CCL4. (c) Cutaneous exposure to the carcinogen DMBA induced IgE production signaling through FcεRI expressed on basophils, which in turn mediated the protection against carcinogenesis. Moreover, αβ T cell-derived IL-4 was critical for IgE production, while tumor-protective IgE also required γδ T cells. DMBA: 7,12-dimethylbenz[a]anthracene; TDLN: tumor draining lymph node; TME: tumor microenvironment; Th2: T helper lymphocyte 2; PDAC: pancreatic ductal adenocarcinoma; CCL: chemokine (C-C motif) ligand; MCP3: monocyte chemotactic protein 3; IL: interleukin; Treg: regulatory T cell; CD: cluster of differentiation; IgE: immunoglobulin E.