Targeting the IL1b Pathway for Cancer Immunotherapy Remodels the Tumor Microenvironment and Enhances Antitumor Immune Responses

High levels of IL1(3 can result in chronic inflammation, which in turn can promote tumor growth and metastasis. Inhibition of IL1(3 could therefore be a promising therapeutic option in the treatment of cancer. Here, the effects of IL1(3 blockade induced by the mAbs canakinumab and gevokizumab were evaluated alone or in combination with docetaxel, anti-programmed cell death protein 1 (anti-PD-1), anti-VEGFoc, and anti-TGF(3 treatment in syngeneic and humanized mouse models of cancers of different origin. Canakinumab and gevokizumab did not show notable efficacy as single-agent therapies; however, IL1(3 blockade enhanced the effectiveness of docetaxel and anti-PD-1. Accompanying these effects, blockade of IL1(3 alone or in combination induced significant remodeling of the tumor microenvironment (TME), with decreased