The switch of glioma-associated TAMs in turn leads to the establishment of an immunosuppressive microenvironment via direct impairment of T-cell activation and proliferation due to the lack of expression of costimulatory molecules (CD40, CD80, and CD86) and the production of low levels of pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) upon TLR stimulation, thus contributes to the failure of T-cell stimulation and proliferation and makes T-cells less capable of mediating tumor cytotoxicity compared with microglia isolated from the normal brain (68, 69). This evidence concerns the gene IL1B and glioma.