BRD4 has a pro-tumorigenic role but non-cell-autonomous mechanisms of BRD4 activation need to be elucidated. Here the authors unravel a mechanism by which CAFs activate BRD4 and induce resistance to BET inhibitors in cancer cells through IL6/IL8 signaling.
B cells have strong clinical significance as drivers of antitumor immunity in triple negative breast cancer. While B cells are known to enhance T cell-mediated tumor killing, we have also uncovered a potential regulatory function, in which they suppress myeloid-derived suppressor cells.
Our study demonstrates that tertiary lymphoid structures (TLS) can form in human glioma, and that agonistic CD40 therapy (αCD40) promotes the formation of TLS in murine glioma models. However, αCD40 also impairs T cell function through the induction of regulatory B cells in the tumor.
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