Figure 3: Multiple layers of regulation of inflammation in tuberculosis . Central panel: interactions of Mycobacterium tuberculosis with professional phagocytes results in activation of several pathways, which concur to induce inflammation. IL-1 necessitates differential requirement for caspase-1 and subsequently inflammasome activation in infected myeloid cells. Left panel: distinct proteinaceous and lipid mediators impact on the fate of the infected cell. Eicosanoids direct cell death (apoptosis vs. necrosis), while abundant TNF-α favors necroptosis and hyper-inflammation. Right panel: genesis of nascent granulomas is controlled by immune and non-immune cells via chemokines and cytokines. Local abundance of proteases and cytokines regulate transition of solid granulomas to necrotic ones. Matrixmetalloproteinases, modulate the extent of tissue damage [36].