Fig. 2

Eosinophil interactions in the tumor microenvironment could be pro-tumorigenic (a) or anti-tumorigenic (b). IFN-γ and TNF-α (to a lesser extent) activate eosinophil tumor suppression mechanism through STAT1 pathway and activate other immune cells, such as CD8 + T cells, Th2 cells, and NK cells to attack primary or metastatic tumors. GM-CSF also positively activates eosinophils by IRF5 transcription factor. IL-33, produced by tumor, immune, or damaged cells, exhibits a plethora of functions that result in tumor regression. In the absence of IFN-γ, eosinophil-recruited Tregs are central to further suppress type 1 immunity and provide a niche suitable for tumor cells’ growth. In multiple myeloma, eosinophils assist myeloma cell growth, especially in earlier stages, by providing IL-6 and APRIL with other cells such as the stromal cells of the bone marrow or osteoclasts (c). Some gut microbiota can exacerbate this situation by stimulating naïve T cell differentiation to Th17 cells that secrete IL-17. Green and red lines point tumor suppression and progression, respectively. Dashed lines indicate cell recruitment. KRG Korean red ginseng, MCP3 monocyte chemotactic protein-3, GZMB granzyme b