Abstract
Drug non-responsiveness is the major reason for the poor prognosis of hormonal receptor-positive breast cancer (ER+/PR+ BCa), particularly the luminal A subtype. However, the underlying mechanism of drug non-responsiveness remains unknown. Flow cytometry and t-SNE analysis followed by ELISA validation of responder and non-responder unveiled lower secretion of IFN-γ, IL-12, and higher levels of IL-6 and TGF-β in CD4+ Tcells (P < 0.001), CD8+ Tcells (P < 0.001), FOXP3+ Tregs (P < 0.001) and CD206+ TAMs (P < 0.001) in non-responders. Treatment of isolated CD206+ TAMs with recombinant IL-6 upregulated the expression of ARG-1 (arginase-1) and subsequent increase of TGF-β+ Tregs (P < 0.001) and IL-6+ Tregs (P < 0.001) in luminal A BCa. Our findings showed IL-6 mediated ARG-1+CD206+ TAMs polarization induced FOXP3+ Tregs infiltration in TME of non-responder in luminal A BCa.
Published Version
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