I redirected M2 macrophages to M1 by treating those with my drug of interest. I am observing upregulated inflammasome activity in these cells. I wonder how this can be explained in the context of solid tumor microenvironment.
As noted in the link by Beatrice, an increased production of pro-inflammatory cytokines by the M1 macrophages activates a gene transcription program (through NF-kB and AP-1 transcription factors) leading to increased cell survival in tumors.