The human breast cancer microenvironment displays features of T helper 2 (Th2) immunity, which
promotes tumor development. We showed that breast cancer cell-derived thymic stromal lymphopoietin
(TSLP), by inducing OX40L expression on DCs, contributes to the Th2 immunity conducive to breast tumor
In order to reprogram the inflammatory pro-tumor Th2 (iTh2) into anti-tumor Th1 microenvironment, we
tested the impact of targeting the innate receptors on DCs to render the resistant to tumor environment.
We show that intratumoral delivery of β-glucan, a natural ligand for dectin-1 expressed on DCs, blocks the
generation of iTh2 cells leading to decreased IL-13 in the tumor microenvironment and prevents breast
cancer development. β-glucan exposed DCs expand CD8+ T cells, which produce higher IFNg, Granzyme A
and Granzyme B, accumulate in the tumors leading to enhanced tumor necrosis in vivo. Our data
demonstrate that exploiting pattern-recognition receptors on tumor-infiltrating DCs enables cancer
We are further exploring the ATACseq and RNAseq approach to understand the regulation of TSLP
production in breast tumor cells and how TSLP alters the infiltrating DCs. It can be novel molecular biology
approaches to decode tumor infiltrating DCs and T cells and define potential targets for immunotherapy.