TMIC-11. ASSOCIATION OF TIM-3/GAL-9 AXIS WITHNLRC4 INFLAMMASOME IN GLIOMA MALIGNANCY: TIM-3/GAL-9 INDUCE THE NLRC4 INFLAMMASOME

Abstract Tim-3/Gal-9 and the NLRC4 inflammasome contribute to glioma progression. However, underlying mechanisms involved are unclear. Here, we observed that expression increased with malignancy found regulate formation activation. inflammasome-related molecule levels WHO grade, this association was correlated low survival. We investigated by genetically regulating Tim-3 its ligand Gal-9. regulation positively inflammasome, NLRC4, caspase-1 expression. did not trigger IL-1 secretion but were strongly activity as they induced programmed cell death in cells. A protein– protein interaction analysis revealed FYN-JAK1-ZNF384 pathways bridges Tim-3/Gal-9. The present study showed associated poor prognosis patients induce proposed a blockade could be beneficial therapy it would reduce inflammatory microenvironment downregulating inflammasome.